the ecg made easy -...

Figure 35. The structure of [M002(N2S2)].

The

ECGMade Easy

For Elsevier

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Content Development Specialist: Helen Leng

Project Manager: Louisa Talbott and Helius

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The

ECGMade Easy

EIGHTH EDITION John R. HamptonDM MA DPhil FRCP FFPM FESC

Emeritus Professor of Cardiology

University of Nottingham, UK

EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2013

© 2013 Elsevier Ltd. All rights reserved.

No part of this publication may be reproduced or transmitted inany form or by any means, electronic or mechanical, includingphotocopying, recording, or any information storage and retrievalsystem, without permission in writing from the publisher. Details onhow to seek permission, further information about the publisher’spermissions policies and our arrangements with organizations suchas the Copyright Clearance Center and the Copyright LicensingAgency, can be found at our website:www.elsevier.com/permissions.

This book and the individual contributions contained in it areprotected under copyright by the publisher (other than as may benoted herein).

First edition 1973 Fifth edition 1997Second edition 1980 Sixth edition 2003Third edition 1986 Seventh edition 2008Fourth edition 1992 Eighth edition 2013

ISBN 978-0-7020-4641-4International ISBN 978-0-7020-4642-1e-book ISBN 978-0-7020-5243-9

British Library Cataloguing in Publication DataA catalogue record for this book is available from the British Library

Library of Congress Cataloging in Publication DataA catalog record for this book is available from the Library of Congress

NoticesKnowledge and best practice in this field are constantly changing.As new research and experience broaden our understanding,changes in research methods, professional practices, or medicaltreatment may become necessary.

Practitioners and researchers must always rely on their ownexperience and knowledge in evaluating and using any information,methods, compounds, or experiments described herein. In usingsuch information or methods they should be mindful of their ownsafety and the safety of others, including parties for whom theyhave a professional responsibility.

With respect to any drug or pharmaceutical products identified,readers are advised to check the most current informationprovided (i) on procedures featured or (ii) by the manufacturer ofeach product to be administered, to verify the recommended doseor formula, the method and duration of administration, andcontraindications. It is the responsibility of practitioners, relying ontheir own experience and knowledge of their patients, to makediagnoses, to determine dosages and the best treatment for eachindividual patient, and to take all appropriate safety precautions.

To the fullest extent of the law, neither the publisher nor the authorassumes any liability for any injury and/or damage to persons orproperty as a matter of products liability, negligence or otherwise, orfrom any use or operation of any methods, products, instructions, orideas contained in the material herein.

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‘medical classic’. The book has been a favourite ofgenerations of medical students and nurses, and ithas changed a lot through progressive editions. Thiseighth edition differs from its predecessors in thatit has been divided into two parts. The first part,‘The Basics’ explains the ECG in the simplestpossible terms, and can be read on its own. Itfocuses on the fundamentals of ECG recording,reporting and interpretation, including the classicalECG abnormalities. The second part, ‘Making themost of the ECG’, has been expanded and dividedinto three chapters. It makes the point that an ECGis simply a tool for the diagnosis and treatment ofpatients, and so has to be interpreted in the light ofthe history and physical examination of the patientfrom whom it was recorded. The variations that mightbe encountered in the situations in which the ECGis most commonly used are considered in separatechapters on healthy subjects (where there is a widerange of normality) and on patients presenting withchest pain, breathlessness, palpitations or syncope.The book is longer than the previous editions, butthat does not mean that the ECG has become moredifficult to understand.

1

v

The ECG Made Easy was first published in 1973,and well over half a million copies of the first seveneditions have been sold. The book has been translatedinto German, French, Spanish, Italian, Portuguese,Polish, Czech, Indonesian, Japanese, Russian andTurkish, and into two Chinese languages. The aimsof this edition are the same as before: the book isnot intended to be a comprehensive textbook ofelectrophysiology, nor even of ECG interpretation –it is designed as an introduction to the ECG formedical students, technicians, nurses and paramedics.It may also provide useful revision for those whohave forgotten what they learned as students.

There really is no need for the ECG to bedaunting: just as most people drive a car withoutknowing much about engines, and gardeners do notneed to be botanists, most people can make full useof the ECG without becoming submerged in itscomplexities. This book encourages the reader toaccept that the ECG is easy to understand and thatits use is just a natural extension of taking the patient’shistory and performing a physical examination.

The first edition of The ECG Made Easy (1973)was described by the British Medical Journal as a

Preface

vi

Preface

previous ones. The expertise of Helius has beencrucial for the new layout of this 8th edition. I am alsograteful to Laurence Hunter, Helen Leng and LouisaTalbott of Elsevier for their continuing support.

The title of The ECG Made Easy was suggestedmore than 30 years ago by the late Tony Mitchell,Foundation Professor of Medicine at the Universityof Nottingham, and many more books have beenpublished with a ‘Made Easy’ title since then. I amgrateful to him and to the many people who havehelped to refine the book over the years, andparticularly to many students for their constructivecriticisms and helpful comments, which have reinforcedmy belief that the ECG really is easy to understand.

John HamptonNottingham, 2013

The ECG Made Easy should help students toprepare for examinations, but for the developmentof clinical competence – and confidence – there is nosubstitute for reporting on large numbers of clinicalrecords. Two companion texts may help those whohave mastered The ECG Made Easy and want toprogress further. The ECG in Practice deals with therelationship between the patient’s history andphysical signs and the ECG, and also with the manyvariations in the ECG seen in health and disease.150 ECG Problems describes 150 clinical cases andgives their full ECGs, in a format that encouragesthe reader to interpret the records and decide ontreatment before looking at the answers.

I am extremely grateful to Mrs Alison Gale whohas not only been a superb copy editor but who hasalso become an expert in ECG interpretation andhas made a major contribution to this edition and to

Part I: The Basics

1. What the ECG is about 3

2. Conduction and its problems 36

3. The rhythm of the heart 56

4. Abnormalities of P waves, QRS complexes and T waves 85

Part II: Making the most of the ECG

5. The ECG in healthy subjects 105

6. The ECG in patients with chest pain or breathlessness 128

7. The ECG in patients with palpitations or syncope 151

8. Now test yourself 174

Index 194

vii

1

Contents

Further reading

The symbol

indicates cross-references to useful information in the book The ECG in Practice, 6th edn.

viii

ECGIP

Before you can use the ECG as an aid todiagnosis or treatment, you have to understandthe basics. Part I of this book explains why theelectrical activity of the heart can be recordedas an ECG, and describes the significance ofthe 12 ECG ‘leads’ that make ‘pictures’ of theelectrical activity seen from different directions.

1

Part I also explains how the ECG can beused to measure the heart rate, to assess thespeed of electrical conduction through differentparts of the heart, and to determine the rhythmof the heart. The causes of common ‘abnormal’ECG patterns are described.

The basicsThe fundamentals of ECG recording,reporting and interpretation

PartI

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What the ECG is about

What to expect from the ECG 3

The electricity of the heart 4

The different parts of the ECG 4

The ECG – electrical pictures 9

The shape of the QRS complex 11

Making a recording – practical points 19

How to report an ECG 32

‘ECG’ stands for electrocardiogram, orelectrocardiograph. In some countries, theabbreviation used is ‘EKG’. Remember:

∑ï By the time you have finished this book,you should be able to say and mean ‘TheECG is easy to understand’.

∑ï Most abnormalities of the ECG areamenable to reason.

WHAT TO EXPECT FROM THE ECG

Clinical diagnosis depends mainly on a patient’shistory, and to a lesser extent on the physicalexamination. The ECG can provide evidence tosupport a diagnosis, and in some cases it iscrucial for patient management. It is, however,important to see the ECG as a tool, and not asan end in itself.

The ECG is essential for the diagnosis, andtherefore the management, of abnormal cardiacrhythms. It helps with the diagnosis of the causeof chest pain, and the proper use of earlyintervention in myocardial infarction dependsupon it. It can help with the diagnosis of thecause of dizziness, syncope and breathlessness.

With practice, interpreting the ECG is amatter of pattern recognition. However, theECG can be analysed from first principles if afew simple rules and basic facts are remembered.This chapter is about these rules and facts.

3

1

The wiring diagram of the heart

THE ELECTRICITY OF THE HEART

The contraction of any muscle is associatedwith electrical changes called ‘depolarization’,and these changes can be detected by electrodesattached to the surface of the body. Since allmuscular contraction will be detected, theelectrical changes associated with contractionof the heart muscle will only be clear if thepatient is fully relaxed and no skeletal musclesare contracting.

Although the heart has four chambers, fromthe electrical point of view it can be thought ofas having only two, because the two atriacontract together (‘depolarization’), and thenthe two ventricles contract together.

THE WIRING DIAGRAM OF THE HEART

The electrical discharge for each cardiac cyclenormally starts in a special area of the rightatrium called the ‘sinoatrial (SA) node’ (Fig. 1.1).Depolarization then spreads through the atrialmuscle fibres. There is a delay whiledepolarization spreads through another specialarea in the atrium, the ‘atrioventricular node’(also called the ‘AV node’, or sometimes just‘the node’). Thereafter, the depolarizationwave travels very rapidly down specializedconduction tissue, the ‘bundle of His’, whichdivides in the septum between the ventriclesinto right and left bundle branches. The leftbundle branch itself divides into two. Withinthe mass of ventricular muscle, conductionspreads somewhat more slowly, throughspecialized tissue called ‘Purkinje fibres’.

THE RHYTHM OF THE HEART

As we shall see later, electrical activation of theheart can sometimes begin in places other thanthe SA node. The word ‘rhythm’ is used to referto the part of the heart which is controlling theactivation sequence. The normal heart rhythm,with electrical activation beginning in the SAnode, is called ‘sinus rhythm’.

THE DIFFERENT PARTS OF THE ECG

The muscle mass of the atria is small comparedwith that of the ventricles, and so the electricalchange accompanying the contraction of the atriais small. Contraction of the atria is associatedwith the ECG wave called ‘P’ (Fig. 1.2). The4


Fig. 1.1

Bundle of His

Left bundle branchRight bundle branch

Sinoatrial node

Atrioventricular node

1The different parts of the ECG

5

ventricular mass is large, and so there is a largedeflection of the ECG when the ventricles aredepolarized: this is called the ‘QRS’ complex.The ‘T’ wave of the ECG is associated with thereturn of the ventricular mass to its restingelectrical state (‘repolarization’).

Shape of the normal ECG, including a

U wave

Fig. 1.2

R

TP U

QS

The letters P, Q, R, S and T were selected inthe early days of ECG history, and were chosenarbitrarily. The P Q, R, S and T deflections areall called waves; the Q, R and S waves togethermake up a complex; and the interval betweenthe S wave and the beginning of the T wave iscalled the ST ‘segment’.

In some ECGs an extra wave can be seen onthe end of the T wave, and this is called a U wave.Its origin is uncertain, though it may representrepolarization of the papillary muscles. If a Uwave follows a normally shaped T wave, it canbe assumed to be normal. If it follows a flattenedT wave, it may be pathological (see Ch. 4).

The different parts of the QRS complex arelabelled as shown in Figure 1.3. If the firstdeflection is downward, it is called a Q wave(Fig. 1.3a). An upward deflection is called an Rwave, regardless of whether it is preceded by aQ wave or not (Figs 1.3b and 1.3c). Anydeflection below the baseline following an Rwave is called an S wave, regardless of whetherthere is a preceding Q wave (Figs 1.3d and 1.3e).

Parts of the QRS complex

Fig. 1.3

Q Q

R

S

R

S

R

Q

R

(a) (b) (c) (d) (e)(a) Q wave. (b, c) R waves.

(d, e) S waves

6


TIMES AND SPEEDS

ECG machines record changes in electricalactivity by drawing a trace on a moving paperstrip. ECG machines run at a standard rate of25 mm/s and use paper with standard-sizedsquares. Each large square (5 mm) represents0.2 second (s), i.e. 200 milliseconds (ms) (Fig.1.4). Therefore, there are five large squares persecond, and 300 per minute. So an ECG event,such as a QRS complex, occurring once perlarge square is occurring at a rate of 300/min.The heart rate can be calculated rapidly byremembering the sequence in Table 1.1.

Just as the length of paper between R wavesgives the heart rate, so the distance between the

different parts of the P–QRS–T complex showsthe time taken for conduction of the electricaldischarge to spread through the different partsof the heart.

The PR interval is measured from thebeginning of the P wave to the beginning of theQRS complex, and it is the time taken forexcitation to spread from the SA node, throughthe atrial muscle and the AV node, down thebundle of His and into the ventricular muscle.Logically, it should be called the PQ interval,but common usage is ‘PR interval’ (Fig. 1.5).

The normal PR interval is 120–220 ms,represented by 3–5 small squares. Most of thistime is taken up by delay in the AV node (Fig. 1.6).

Relationship between the squares on ECG paper and time. Here, there is one QRS complex

per second, so the heart rate is 60 beats/min

Fig. 1.4

1 small square represents0.04 s (40 ms)

1 large square represents0.2 s (200 ms)

R–R interval:5 large squares represent 1 s

The duration of the QRS complex showshow long excitation takes to spread throughthe ventricles. The QRS complex duration isnormally 120 ms (represented by three small

1The different parts of the ECG

7

If the PR interval is very short, either theatria have been depolarized from close to the AV node, or there is abnormally fastconduction from the atria to the ventricles.

Table 1.1 Relationship between the number of

large squares between successive R waves and

the heart rate

R–R interval Heart rate

(large squares) (beats/min)

1 300

2 150

3 100

4 75

5 60

6 50

The components of the ECG complex

Fig. 1.5

R

STsegment

QT interval

PR intervalQRS

TP

QS

U

PR0.18 s (180 ms)

QRS0.12 s (120 ms)

Normal PR interval and QRS complex

Fig. 1.6

Normal PR interval and prolonged QRS complex

8


calibrated. A standard signal of 1 millivolt (mV)should move the stylus vertically 1 cm (twolarge squares) (Fig. 1.8), and this ‘calibration’signal should be included with every record.

PR0.16 s (160 ms)

QRS0.20 s (200 ms)

Fig. 1.7

squares) or less, but any abnormality ofconduction takes longer, and causes widenedQRS complexes (Fig. 1.7). Remember that theQRS complex represents depolarization, notcontraction, of the ventricles – contraction isproceeding during the ECG’s ST segment.

The QT interval varies with the heart rate. Itis prolonged in patients with some electrolyteabnormalities, and more importantly it isprolonged by some drugs. A prolonged QTinterval (greater than 450 ms) may lead toventricular tachycardia.

CALIBRATION

A limited amount of information is given bythe height of the P waves, QRS complexes andT waves, provided the machine is properly

1 cm

Calibration of the ECG recording

Fig. 1.8

recorder by wires. One electrode is attached toeach limb, and six to the front of the chest.

The ECG recorder compares the electricalactivity detected in the different electrodes,and the electrical picture so obtained is called a‘lead’. The different comparisons ‘look at’ theheart from different directions. For example,when the recorder is set to ‘lead I’ it is comparingthe electrical events detected by the electrodesattached to the right and left arms. Each leadgives a different view of the electrical activityof the heart, and so a different ECG pattern.Strictly, each ECG pattern should be called‘lead ...’, but often the word ‘lead’ is omitted.

The ECG is made up of 12 characteristicviews of the heart, six obtained from the ‘limb’leads (I, II, III, VR, VL, VF) and six from the‘chest’ leads (V1–V6). It is not necessary toremember how the leads (or views of the heart)are derived by the recorder, but for those wholike to know how it works, see Table 1.2. Theelectrode attached to the right leg is used as anearth, and does not contribute to any lead.

THE 12-LEAD ECG

ECG interpretation is easy if you remember thedirections from which the various leads look atthe heart. The six ‘standard’ leads, which arerecorded from the electrodes attached to thelimbs, can be thought of as looking at the heartin a vertical plane (i.e. from the sides or thefeet) (Fig. 1.9).

THE ECG – ELECTRICAL PICTURES

The word ‘lead’ sometimes causes confusion.Sometimes it is used to mean the pieces of wirethat connect the patient to the ECG recorder.Properly, a lead is an electrical picture of theheart.

The electrical signal from the heart isdetected at the surface of the body throughelectrodes, which are joined to the ECG

1The ECG – electrical pictures

9

Table 1.2 ECG leads

Lead Comparison of electrical activity

I LA and RA

II LL and RA

III LL and LA

VR RA and average of (LA + LL)

VL LA and average of (RA + LL)

VF LL and average of (LA + RA)

V1 V1 and average of (LA + RA + LL)






Key: LA, left arm; RA, right arm; LL, left leg.

10


VRVL

VF

III II

I

The ECG patterns recorded by the six ‘standard’ leads

Fig. 1.9

Leads I, II and VL look at the left lateralsurface of the heart, leads III and VF at theinferior surface, and lead VR looks at the rightatrium.

The six V leads (V1–V6) look at the heart in a horizontal plane, from the front and the

left side. Thus, leads V1 and V2 look at theright ventricle, V3 and V4 look at the septumbetween the ventricles and the anterior wall ofthe left ventricle, and V5 and V6 look at theanterior and lateral walls of the left ventricle(Fig. 1.10).

1The shape of the QRS complex

11

As with the limb leads, the chest leads eachshow a different ECG pattern (Fig. 1.11). Ineach lead the pattern is characteristic, beingsimilar in individuals who have normal hearts.

The cardiac rhythm is identified fromwhichever lead shows the P wave most clearly –usually lead II. When a single lead is recordedsimply to show the rhythm, it is called a‘rhythm strip’, but it is important not to makeany diagnosis from a single lead, other thanidentifying the cardiac rhythm.

The relationship between the six chest leads and the heart

Fig. 1.10

V6

V5

V4

V3V2V1

LVRV

THE SHAPE OF THE QRS COMPLEX

We now need to consider why the ECG has acharacteristic appearance in each lead.

THE QRS COMPLEX IN THE LIMB LEADS

The ECG machine is arranged so that when adepolarization wave spreads towards a lead thestylus moves upwards, and when it spreads awayfrom the lead the stylus moves downwards.

12


V6V5V4V3V2V1

The ECG patterns recorded by the chest leads

Fig. 1.11

Depolarization spreads through the heart inmany directions at once, but the shape of theQRS complex shows the average direction inwhich the wave of depolarization is spreadingthrough the ventricles (Fig. 1.12).

If the QRS complex is predominantly upward,or positive (i.e. the R wave is greater than the Swave), the depolarization is moving towards that

lead (Fig. 1.12a). If predominantly downward,or negative (the S wave is greater than the Rwave), the depolarization is moving away fromthat lead (Fig. 1.12b). When the depolarizationwave is moving at right angles to the lead, theR and S waves are of equal size (Fig. 1.12c). Qwaves, when present, have a special significance,which we shall discuss later.


13

Depolarization and the shape of the QRS complex

Fig. 1.12

R

S

R

S

R

S

(a) (b) (c)

Depolarization (a) moving towards the lead,

causing a predominantly upward QRS complex;

(b) moving away from the lead, causing a

predominantly downward QRS complex;

and (c) at right angles to the lead, generating

equal R and S waves

14


THE CARDIAC AXIS

Leads VR and II look at the heart from oppositedirections. When seen from the front, thedepolarization wave normally spreads throughthe ventricles from 11 o’clock to 5 o’clock, sothe deflections in lead VR are normally mainlydownward (negative) and in lead II mainlyupward (positive) (Fig. 1.13).

The average direction of spread of thedepolarization wave through the ventricles asseen from the front is called the ‘cardiac axis’.It is useful to decide whether this axis is in a

normal direction or not. The direction of theaxis can be derived most easily from the QRScomplex in leads I, II and III.

A normal 11 o’clock–5 o’clock axis meansthat the depolarizing wave is spreading towardsleads I, II and III, and is therefore associatedwith a predominantly upward deflection in allthese leads; the deflection will be greater inlead II than in I or III (Fig. 1.14).

When the R and S waves of the QRS complexare equal, the cardiac axis is at right angles tothat lead.

The cardiac axis

Fig. 1.13

VR

VL

VFIII

II

I

The normal axis

Fig. 1.14

III II

I


15

If the right ventricle becomes hypertrophied,it has more effect on the QRS complex thanthe left ventricle, and the average depolarizationwave – the axis – will swing towards the right.The deflection in lead I becomes negative(predominantly downward) because depolarizationis spreading away from it, and the deflection inlead III becomes more positive (predominantlyupward) because depolarization is spreadingtowards it (Fig. 1.15). This is called ‘right axisdeviation’. It is associated mainly with pulmonaryconditions that put a strain on the right side ofthe heart, and with congenital heart disorders.

When the left ventricle becomes hypertrophied,it exerts more influence on the QRS complexthan the right ventricle. Hence, the axis mayswing to the left, and the QRS complexbecomes predominantly negative in lead III(Fig. 1.16). ‘Left axis deviation’ is notsignificant until the QRS complex deflection isalso predominantly negative in lead II.Although left axis deviation can be due toexcess influence of an enlarged left ventricle, infact this axis change is usually due to aconduction defect rather than to increased bulkof the left ventricular muscle (see Ch. 2).

Right axis deviation

Fig. 1.15

III II

I

Left axis deviation

Fig. 1.16

III II

I

The cardiac axis is sometimes measured indegrees (Fig. 1.17), though this is not clinicallyparticularly useful. Lead I is taken as looking atthe heart from 0°; lead II from +60°; lead VFfrom +90°; and lead III from +120°. Leads VLand VR look from –30° and –150°, respectively.

The normal cardiac axis is in the range –30°to +90°. If in lead II the S wave is greater thanthe R wave, the axis must be more than 90°away from lead II. In other words, it must be

at a greater angle than –30°, and closer to thevertical (see Figs 1.16 and 1.17), and left axisdeviation is present. Similarly, if the size of theR wave equals that of the S wave in lead I, theaxis is at right angles to lead I or at +90°. Thisis the limit of normality towards the ‘right’. Ifthe S wave is greater than the R wave in leadI, the axis is at an angle of greater than +90°,and right axis deviation is present (Fig. 1.15).

WHY WORRY ABOUT THE CARDIAC AXIS?

Right and left axis deviation in themselves areseldom significant – minor degrees occur in tall,thin individuals and in short, fat individuals,respectively. However, the presence of axisdeviation should alert you to look for othersigns of right and left ventricular hypertrophy(see Ch. 4). A change in axis to the right maysuggest a pulmonary embolus, and a change tothe left indicates a conduction defect.

THE QRS COMPLEX IN THE V LEADS

The shape of the QRS complex in the chest (V)leads is determined by two things:

∑ The septum between the ventricles isdepolarized before the walls of theventricles, and the depolarization wavespreads across the septum from left to right.

∑ In the normal heart there is more muscle inthe wall of the left ventricle than in that ofthe right ventricle, and so the left ventricleexerts more influence on the ECG patternthan does the right ventricle.16


The cardiac axis and lead angles

Fig. 1.17

VR–150°

VL–30°

+90° VF

+120° III

+60° II

0° I

Limit of the normalcardiac axis

–90°

–180°+180°

Left axisdeviation

Right axisdeviation


17

Leads V1 and V2 look at the right ventricle;leads V3 and V4 look at the septum; and leadsV5 and V6 at the left ventricle (Fig. 1.10).

In a right ventricular lead the deflection is firstupwards (R wave) as the septum is depolarized.In a left ventricular lead the opposite pattern is seen: there is a small downward deflection(‘septal’ Q wave) (Fig. 1.18).

In a right ventricular lead there is then adownward deflection (S wave) as the main musclemass is depolarized – the electrical effects in thebigger left ventricle (in which depolarization isspreading away from a right ventricular lead)outweighing those in the smaller right ventricle.

In a left ventricular lead there is an upwarddeflection (R wave) as the ventricular muscle isdepolarized (Fig. 1.19).

When the whole of the myocardium isdepolarized, the ECG trace returns to thebaseline (Fig. 1.20).

The QRS complex in the chest leads showsa progression from lead Vl, where it ispredominantly downward, to lead V6, where itis predominantly upward (Fig. 1.21). The‘transition point’, where the R and S waves areequal, indicates the position of the interventricularseptum.

Q

R

V6

V1

Shape of the QRS complex: first stage

Fig. 1.18

S

R

V6

V1

Shape of the QRS complex: second stage

Fig. 1.19

18


S

Q

R

R

V6

V1

Shape of the QRS complex: third stage

Fig. 1.20

V6V5V4V3V2V1

The ECG patterns recorded by the chest leads

Fig. 1.21

1Making a recording – practical points

WHY WORRY ABOUT THE TRANSITIONPOINT?

If the right ventricle is enlarged, and occupiesmore of the precordium than is normal, thetransition point will move from its normalposition of leads V3/V4 to leads V4/V5 orsometimes leads V5/V6. Seen from below, theheart can be thought of as having rotated in aclockwise direction. ‘Clockwise rotation’ in theECG is characteristic of chronic lung disease.

MAKING A RECORDING – PRACTICAL

POINTS

Now that you know what an ECG should looklike, and why it looks the way it does, we needto think about the practical side of making arecording. Some, but not all, ECG recordersproduce a ‘rhythm strip’, which is a continuousrecord, usually of lead II. This is particularlyuseful when the rhythm is not normal. Thenext series of ECGs were all recorded from ahealthy subject whose ‘ideal’ ECG is shown inFigure 1.22.

19

It is really important to make sure that theelectrode marked LA is indeed attached to theleft arm, RA to the right arm and so on. If thelimb electrodes are wrongly attached, the12-lead ECG will look very odd (Fig. 1.23). Itis possible to interpret the ECG, but it is easierto recognize that there has been a mistake, andto repeat the recording.

Reversal of the leg electrodes does not makemuch difference to the ECG.

The chest electrodes need to be accuratelypositioned, so that abnormal patterns in the Vleads can be identified, and so that recordstaken on different occasions can be compared.Identify the second rib interspace by feeling forthe sternal angle – this is the point where themanubrium and the body of the sternum meet,and there is usually a palpable ridge where thebody of the sternum begins, angling downwardsin comparison to the manubrium. The secondrib is attached to the sternum at the angle, andthe second rib space is just below this. Havingidentified the second space, feel downwards forthe third and then the fourth rib spaces, overwhich the electrodes for V1 and V2 are attached,to the right and left of the sternum, respectively.

20


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 1.22

A good record of a normal ECGNote

∑ The upper three traces show the six limb leads (I, II, III, VR, VL, VF) and then the six chest leads

∑ The bottom trace is a ‘rhythm strip’, entirely recorded from lead II (i.e. no lead changes)

∑ The trace is clear, with P waves, QRS complexes and T waves visible in all leads


21

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.23

The effect of reversing the electrodes attached to the left and right armsNote

∑ Compare with Figure 1.22, correctly recorded from the same patient

∑ Inverted P waves in lead I

∑ Abnormal QRS complexes and T waves in lead I

∑ Upright T waves in lead VR are most unusual

22


V6

Midclavicular line

V5V4V3V2V1

Anterior axillary line

Midaxillary line

4th

5th

The positions of the chest leads: note the fourth and fifth rib spaces

Fig. 1.24

The other electrodes are then placed as shownin Figure 1.24, with V4 in the midclavicular line(the imaginary vertical line starting from themidpoint of the clavicle); V5 in the anterioraxillary line (the line starting from the fold ofskin that marks the front of the armpit); and V6in the midaxillary line.

Good electrical contact between theelectrodes and the skin is essential. The effectson the ECG of poor skin contact are shown inFigure 1.25. The skin must be clean and dry –in any patient using creams or moisturizers(such as patients with skin disorders) it shouldbe cleaned with alcohol; the alcohol must be


23

wiped off before the electrodes are applied.Abrasion of the skin is essential; in mostpatients all that is needed is a rub with a papertowel. In exercise testing, when the patient islikely to become sweaty, abrasive pads may beused – for these tests it is worth spending timeto ensure good contact, because in many cases

the ECG becomes almost unreadable towardsthe end of the test. Hair is a poor conductor ofthe electrical signal and prevents the electrodesfrom sticking to the skin. Shaving may bepreferable, but patients may not like this – ifthe hair can be parted and firm contact madewith the electrodes, this is acceptable. After

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 1.25

The effect of poor electrode contactNote

∑ Bizarre ECG patterns

∑ In the rhythm strip (lead II), the patterns vary

24


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.26

The effect of electrical interferenceNote

∑ Regular sharp high-frequency spikes, giving the appearance of a thick baseline

shaving, the skin will need to be cleaned withalcohol or a soapy wipe.

Even with the best of ECG recorders, electricalinterference can cause regular oscillation in theECG trace, at first sight giving the impressionof a thickened baseline (Fig. 1.26). It can be

extremely difficult to work out where electricalinterference may be coming from, but thinkabout electric lights, and electric motors on bedsand mattresses.

ECG recorders are normally calibrated sothat 1 mV of signal causes a deflection of 1 cm


25

on the ECG paper, and a calibration signalusually appears at the beginning (and often alsoat the end) of a record. If the calibration settingis wrong, the ECG complexes will look toolarge or too small (Figs 1.27 and 1.28). Largecomplexes may be confused with left ventricular

hypertrophy (see Ch. 4), and small complexesmight suggest that there is something like apericardial effusion reducing the electricalsignal from the heart. So, check the calibration.

ECG recorders are normally set to run at apaper speed of 25 mm/s, but they can be altered

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.27

The effect of over-calibrationNote

∑ The calibration signal (1 mV) at the left-hand end of each line causes a deflection of 2 cm

∑ All the complexes are large compared with an ECG recorded with the correct calibration (e.g. Fig. 1.22,

in which 1 mV causes a deflection of 1 cm)

26


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.28

The effect of under-calibrationNote

∑ The calibration signal (1 mV) causes a deflection of 0.5 cm

∑ All the complexes are small


27

to run at slower speeds (which make thecomplexes appear spiky and bunched together)or to 50 mm/s (Figs 1.29 and 1.30). The fasterspeed is used regularly in some Europeancountries, and makes the ECG look ‘spread out’.In theory this can make the P wave easier to see,but in fact flattening out the P wave tends tohide it, and so this fast speed is seldom useful.

ECG recorders are ‘tuned’ to the electricalfrequency generated by heart muscle, but theywill also detect the contraction of skeletalmuscle. It is therefore essential that a patient isrelaxed, warm and lying comfortably – if theyare moving or shivering, or have involuntary

movements such as those of Parkinson’s disease,the recorder will pick up a lot of muscularactivity, which in extreme cases can mask theECG (Figs 1.31 and 1.32).

So, the ECG recorder will do most of thework for you – but remember to:

∑ï attach the electrodes to the correct limbs∑ï ensure good electrical contact∑ï check the calibration and speed settings ∑ï get the patient comfortable and relaxed.

Then just press the button, and the recorderwill automatically provide a beautiful 12-leadECG.

28


VRI

VLII

VFIII

Fig. 1.29

Normal ECG recorded with a paper speed of 50 mm/sNote

∑ A paper speed of 50 mm/s is faster than normal

∑ Long interval between QRS complexes gives the impression of a slow heart rate

∑ Widened QRS complexes

∑ Apparently very long QT interval


29

V1 V4

V2 V5

V3 V6

30


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.30

A normal ECG recorded with a paper speed of 12.5 mm/sNote

∑ A paper speed of 12.5 mm/s is slower than normal

∑ QRS complexes are close together, giving the impression of a rapid heart rate

∑ P waves, QRS complexes and T waves are all narrow and ‘spiky’


31

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.31

An ECG from a subject who is not relaxedNote

∑ Same subject as in Figs 1.22–1.30

∑ The baseline is no longer clear, and is replaced by a series of sharp irregular spikes – particularly

marked in the limb leads

32


HOW TO REPORT AN ECG

Many ECG recorders automatically provide areport, and in these reports the heart rate andthe conducting intervals are usually accuratelymeasured. However, the description of therhythm and of the QRS and T patterns shouldbe regarded with suspicion. Recorders tend to‘over-report’, and to describe abnormalities wherenone exist: it is much better to be confident inyour own reporting.

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.32

The effect of shiveringNote

∑ The spikes are more exaggerated than when a patient is not relaxed

∑ The sharp spikes are also more synchronized, because the skeletal muscle groups are contracting together

∑ The effects of skeletal muscle contraction almost obliterate those of cardiac muscle contraction in leads

I, II and III

You now know enough about the ECG tounderstand the basis of a report. This shouldtake the form of a description followed by aninterpretation.

The description should always be given inthe same sequence:

1. Rhythm2. Conduction intervals 3. Cardiac axis4. A description of the QRS complexes5. A description of the ST segments and T waves.

1How to report an ECG

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 1.33

Variant of a normal ECGNote

∑ Sinus rhythm, rate 50/min

∑ Normal PR interval (100 ms)

∑ Normal QRS complex duration (120 ms)

∑ Normal cardiac axis

∑ Normal QRS complexes

33

∑ Normal T waves (an inverted T wave in lead VR is normal)

∑ Prominent (normal) U waves in leads V2–V4

Interpretation

∑ Normal ECG

Reporting a series of totally normal findingsis possibly pedantic, and in real life this isfrequently not done. However, you must thinkabout all the findings every time you interpretan ECG.

The interpretation of an ECG indicateswhether the record is normal or abnormal: if

abnormal, the underlying pathology needs tobe identified. One of the main problems ofECG reporting is that there is quite a lot ofvariation in the normal ECG. Figures 1.33 and1.34 are examples of 12-lead ECGs showingnormal variants.

V1 V4VRI

V2 V5VLII

V3 V6VFIII

34


Fig. 1.34

Variant of a normal ECGNote


∑ Normal PR interval (200 ms)

∑ Normal QRS complex duration (120 ms)

∑ Right axis deviation (prominent S wave in lead I)


∑ Normal ST segments and T waves

Interpretation

∑ Normal ECG – apart from right axis deviation,

which could be normal in a tall, thin person

1Reminders

35

REMINDERS

BASIC PRINCIPLES

∑ The cardiac axis is the average direction ofspread of depolarization as seen from thefront, and is estimated from leads I, II and III.

∑ The chest or V leads look at the heart fromthe front and the left side in a horizontalplane. Lead V1 is positioned over the rightventricle, and lead V6 over the left ventricle.

∑ The septum is depolarized from the leftside to the right.

∑ In a normal heart the left ventricle exertsmore influence on the ECG than the rightventricle.

∑ Unfortunately, there are a lot of minorvariations in ECGs which are consistentwith perfectly normal hearts. Recognizingthe limits of normality is one of the maindifficulties of ECG interpretation.

∑ The ECG results from electrical changesassociated with activation (depolarization)first of the atria and then of the ventricles.

∑ Atrial depolarization causes the P wave.

∑ Ventricular depolarization causes the QRScomplex. If the first deflection is downward,it is a Q wave. Any upward deflection is an R wave. A downward deflection after an Rwave is an S wave.

∑ When the depolarization wave spreadstowards a lead, the deflection is predominantlyupward. When the wave spreads away froma lead, the deflection is predominantlydownward.

∑ The six limb leads (I, II, III, VR, VL and VF) lookat the heart from the sides and the feet in avertical plane.

R

Q S

ECGIP

For more on

normal variants

of the ECG,

see Ch. 1

36

2 Conduction andits problems

Conduction problems in the AV node and

His bundle 37

Conduction problems in the right and left

bundle branches – bundle branch block 43

Conduction problems in the distal parts

of the left bundle branch 49

What to do 54

We have already seen that electricaldepolarization normally begins in the sinoatrial(SA) node, and that a wave of depolarizationspreads outwards through the atrial muscle tothe atrioventricular (AV) node, and thencedown the His bundle and its branches to the

ventricles. The conduction of this wave frontcan be delayed or blocked at any point.However, conduction problems are simple toanalyse, provided you keep the wiring diagramof the heart constantly in mind (Fig. 2.1).

We can think of conduction problems in theorder in which the depolarization wave normallyspreads: SA node Æ AV node Æ His bundle Æbundle branches. Remember in all that followsthat we are assuming depolarization begins inthe normal way in the SA node.

The rhythm of the heart is best interpretedfrom whichever ECG lead shows the P wavemost clearly. This is usually, but not always, leadII or lead V1. You can assume that all the‘rhythm strips’ in this book were recorded fromone of these leads.

2Problems in the AV node and His bundle

37

The wiring diagram of the heart

CONDUCTION PROBLEMS IN THE AV

NODE AND HIS BUNDLE

The time taken for the spread of depolarizationfrom the SA node to the ventricular muscle is shown by the PR interval (see Ch. 1), and isnot normally greater than 220 ms (six smallsquares).

Interference with the conduction processcauses the phenomenon called ‘heart block’.

FIRST DEGREE HEART BLOCK

If each wave of depolarization that originates inthe SA node is conducted to the ventricles, butthere is delay somewhere along the conductionpathway, then the PR interval is prolonged.This is called ‘first degree heart block’ (Fig. 2.2).

First degree heart block is not in itselfimportant, but it may be a sign of coronary arterydisease, acute rheumatic carditis, digoxin toxicityor electrolyte disturbances.

Fig. 2.1

Bundle of His

Left bundle branch

Right bundle branch

Sinoatrial node

Atrioventricular node

depolarization without a subsequentventricular depolarization. This is calledthe ‘Mobitz type 2’ phenomenon (Fig. 2.4).

3. There may be alternate conducted and nonconducted atrial beats (or oneconducted atrial beat and then two orthree nonconducted beats), giving twice (or three or four times) as many P waves as QRS complexes. This is called ‘2:1’(‘two to one’), ‘3:1’ (‘three to one’) or ‘4:1’ (‘four to one’) conduction (Fig. 2.5).

It is important to remember that, as with anyother rhythm, a P wave may only show itself asa distortion of a T wave (Fig. 2.6).

38

Conduction and its problems

SECOND DEGREE HEART BLOCK

Sometimes excitation completely fails to passthrough the AV node or the bundle of His.When this occurs intermittently, ‘second degreeheart block’ is said to exist. There are threevariations of this:

1. There may be progressive lengthening of thePR interval and then failure of conductionof an atrial beat, followed by a conductedbeat with a shorter PR interval and then a repetition of this cycle. This is the‘Wenckebach’ or ‘Mobitz type 1’phenomenon (Fig. 2.3).

2. Most beats are conducted with a constantPR interval, but occasionally there is atrial

First degree heart block

Fig. 2.2

PR360 ms

Note

∑ One P wave per QRS complex

∑ PR interval 360 ms


Second degree heart block (Mobitz type 2)

Fig. 2.4

Note

∑ PR interval of the conducted beats is

constant

∑ One P wave is not followed by a QRS

complex

39

Second degree heart block (Wenckebach (Mobitz type 1))

Fig. 2.3

P P260 ms 280 ms 320 ms 260 ms 280 ms 320 ms

Note

∑ Progressive lengthening of the

PR interval

∑ One nonconducted P wave

∑ Next conducted beat has a shorter

PR interval than the preceding

conducted beat

∑ As with any other rhythm, a P wave

may only show itself as a distortion

of a T wave

The underlying causes of second degree heartblock are the same as those of first degree block.The Wenckebach phenomenon is usually benign,

but Mobitz type 2 block and 2:1, 3:1 or 4:1block may herald ‘complete,’ or ‘third degree’,heart block.

40


Second degree heart block (2:1 type)

Fig. 2.6

P

Note

∑ P wave in the T wave can be

identified because of its regularity

Second degree heart block (2:1 type)

Fig. 2.5

P

Note

∑ Two P waves per QRS complex

∑ Normal, and constant, PR interval in

the conducted beats

THIRD DEGREE HEART BLOCK

Complete heart block (third degree block) is saidto occur when atrial contraction is normal but nobeats are conducted to the ventricles (Fig. 2.7).When this occurs the ventricles are excited bya slow ‘escape mechanism’ (see Ch. 3), from adepolarizing focus within the ventricular muscle.

Complete block is not always immediatelyobvious in a 12-lead ECG, where there may be


only a few QRS complexes per lead (e.g. seeFig. 2.8). You have to look at the PR interval inall the leads to see that there is no consistency.

Complete heart block may occur as an acutephenomenon in patients with myocardialinfarction (when it is usually transient) or itmay be chronic, usually due to fibrosis aroundthe bundle of His. It may also be caused by theblock of both bundle branches.

41

Third degree heart block

Fig. 2.7

PNote

∑ P wave rate 90/min

∑ No relationship between P waves

and QRS complexes

∑ QRS complex rate 36/min

∑ Abnormally shaped QRS complexes,

because of abnormal spread of

depolarization from a ventricular

focus

V1 V4VRI

V2 V5VLII

V3 V6VFIII

42


Fig. 2.8

Complete heart blockNote

∑ Sinus rhythm, but no P waves are conducted

∑ Right axis deviation

∑ Broad QRS complexes (duration 160 ms)

∑ Right bundle branch block pattern

∑ In this case the cause of the block could not be

determined, though in most patients it results

from fibrosis of the bundle of His

2Problems in the right and left bundle branches

CONDUCTION PROBLEMS IN THE

RIGHT AND LEFT BUNDLE BRANCHES –

BUNDLE BRANCH BLOCK

If the depolarization wave reaches theinterventricular septum normally, the intervalbetween the beginning of the P wave and the firstdeflection in the QRS complex (the PR interval)will be normal. However, if there is abnormalconduction through either the right or leftbundle branches (‘bundle branch block’) therewill be a delay in the depolarization of part ofthe ventricular muscle. The extra time taken fordepolarization of the whole of the ventricularmuscle causes widening of the QRS complex.

In the normal heart, the time taken for thedepolarization wave to spread from theinterventricular septum to the furthest part ofthe ventricles is less than 120 ms, representedby three small squares of ECG paper. If theQRS complex duration is greater than 120 ms,then conduction within the ventricles musthave occurred by an abnormal, and thereforeslower, pathway.

A wide QRS complex can therefore indicatebundle branch block, but widening also occursif depolarization begins within the ventricularmuscle itself (see Ch. 3). However, remember

that in sinus rhythm with bundle branch block,normal P waves are present with a constant PRinterval. We shall see that this is not the casewith rhythms beginning in the ventricles.

Block of both bundle branches has the sameeffect as block of the His bundle, and causescomplete (third degree) heart block.

Right bundle branch block (RBBB) oftenindicates problems in the right side of the heart,but RBBB patterns with a QRS complex of normalduration are quite common in healthy people.

Left bundle branch block (LBBB) is alwaysan indication of heart disease, usually of the leftventricle.

It is important to recognize when bundlebranch block is present, because LBBB preventsany further interpretation of the cardiogram,and RBBB can make interpretation difficult.

The mechanism underlying the ECG patternsof RBBB and LBBB can be worked out fromfirst principles. Remember (see Ch. 1):

∑ The septum is normally depolarized fromleft to right.

∑ The left ventricle, having the greater musclemass, exerts more influence on the ECGthan does the right ventricle.

∑ Excitation spreading towards a lead causesan upward deflection within the ECG.

43

of the failure of the normal conducting pathway.The right ventricle therefore depolarizes afterthe left. This causes a second R wave (R1) inlead V1, and a wide and deep S wave, andconsequently a wide QRS complex, in lead V6(Fig. 2.11).

An ‘RSR1’ pattern, with a QRS complex ofnormal width (less than 120 ms), is sometimescalled ‘partial right bundle branch block’. It isseldom of significance, and can be consideredto be a normal variant.

V1

V6

R

Q

R

S

RIGHT BUNDLE BRANCH BLOCK

In RBBB, no conduction occurs down the rightbundle branch but the septum is depolarizedfrom the left side as usual, causing an R wave ina right ventricular lead (V1) and a small Q wavein a left ventricular lead (V6) (Fig. 2.9).

Excitation then spreads to the left ventricle,causing an S wave in lead V1 and an R wave inlead V6 (Fig. 2.10).

It takes longer than in a normal heart forexcitation to reach the right ventricle because

44


Conduction in right bundle branch block:

first stage

Fig. 2.9

V6

V1

Q

R


second stage

Fig. 2.10

LEFT BUNDLE BRANCH BLOCK

If conduction down the left bundle branch fails,the septum becomes depolarized from right toleft, causing a small Q wave in lead V1, and anR wave in lead V6 (Fig. 2.12).

The right ventricle is depolarized before theleft, so despite the smaller muscle mass there isan R wave in lead V1 and an S wave (oftenappearing only as a notch) in lead V6 (Fig. 2.13).Remember that any upward deflection, however


45


third stage

Fig. 2.11

V6

V1

R

SQ

R R1

S

small, is an R wave, and any downwarddeflection, however small, following an R waveis called an S wave.

Subsequent depolarization of the left ventriclecauses an S wave in lead V1 and another Rwave in lead V6 (Fig. 2.14).

LBBB is associated with T wave inversion inthe lateral leads (I, VL and V5–V6), though notnecessarily in all of these.

Conduction in left bundle branch block:

first stage

Fig. 2.12

V6

V1

R

Q

46



second stage

Fig. 2.13

V6

V1

S

R

R

Q


third stage

Fig. 2.14

V6

V1

R

S

REMINDERS

BUNDLE BRANCH BLOCK

∑ RBBB is best seen in lead V1, where there is an RSR1 pattern (Fig. 2.15).

∑ LBBB is best seen in lead V6, where there is a broad QRS complex with a notched top, whichresembles the letter ‘M’ and is therefore known as an ‘M’ pattern (Fig. 2.16). The complete picture,with a ‘W’ pattern in lead V1, is often not fully developed.

V1 V4VRI

V2 V5VLII

V3 V6VFIII


47

Fig. 2.15

Sinus rhythm with right bundle branch blockNote


∑ Normal PR interval


∑ Wide QRS complexes (160 ms)

∑ RSR1 pattern in lead V1 and deep, wide S waves in lead V6


V1 V4VRI

V2 V5VLII

V3 V6VFIII

48


Fig. 2.16

Sinus rhythm with left bundle branch blockNote




∑ Wide QRS complexes (160 ms)

∑ M pattern in the QRS complexes, best seen in leads I, VL, V5 and V6

∑ Inverted T waves in leads I, II, VL

2Problems in the distal parts of the left bundle branch

49

The three pathways of the depolarization wave

Fig. 2.17

Bundle of His

Left bundle branch

Right bundlebranch

AV node

Posterior fascicle

Anterior fascicle

CONDUCTION PROBLEMS IN

THE DISTAL PARTS OF THE LEFT

BUNDLE BRANCH

At this point it is worth considering in a littlemore detail the anatomy of the branches of theHis bundle. The right bundle branch has nomain divisions, but the left bundle branch hastwo – the anterior and posterior ‘fascicles’. Thedepolarization wave therefore spreads into theventricles by three pathways (Fig. 2.17).

The cardiac axis (see Ch. 1) depends on theaverage direction of depolarization of theventricles. Because the left ventricle containsmore muscle than the right, it has moreinfluence on the cardiac axis (Fig. 2.18).

If the anterior fascicle of the left bundlebranch fails to conduct, the left ventricle has tobe depolarized through the posterior fascicle, andso the cardiac axis rotates upwards (Fig. 2.19).

Left axis deviation is therefore due to leftanterior fascicular block, or ‘left anteriorhemiblock’ (Fig. 2.20).

50


Effect of normal conduction on the cardiac axis

Fig. 2.18

Normal axis

Effect of left anterior fascicular block on the cardiac axis

Fig. 2.19

Left axis deviation

V1 V4VRI

V2 V5VLII

V3 V6VFIII


51

The posterior fascicle of the left bundle isonly rarely selectively blocked, in ‘left posteriorhemiblock’, but if this does occur the ECGshows right axis deviation.

When the right bundle branch is blocked, thecardiac axis usually remains normal, becausethere is normal depolarization of the leftventricle with its large muscle mass (Fig. 2.21).

However, if both the right bundle branchand the left anterior fascicle are blocked, the

ECG shows RBBB and left axis deviation (Fig.2.22). This is sometimes called ‘bifascicularblock’, and this ECG pattern obviously indicateswidespread damage to the conducting system(Fig. 2.23).

If the right bundle branch and both fasciclesof the left bundle branch are blocked, completeheart block occurs just as if the main His bundlehad failed to conduct.

Fig. 2.20

Sinus rhythm with left axis deviation (otherwise normal)Note


∑ Left axis deviation: QRS complex upright in lead I, but downward (dominant S wave) in leads II and III

∑ Normal QRS complexes, ST segments and T waves

52


Lack of effect of right bundle branch block on the cardiac axis

Fig. 2.21

RBBB

Effect of right bundle branch block and left anterior hemiblock on the cardiac axis

Fig. 2.22

Left axis deviation

RBBB

I VR V1 V4

II VL V2 V5

III VF V3 V6


53

Fig. 2.23

Bifascicular blockNote


∑ Left axis deviation (dominant S wave in leads II and III)

∑ Right bundle branch block (RSR1 pattern in lead V1, and deep, wide S wave in lead V6)

54


WHAT TO DO

Always remember that it is the patient who shouldbe treated, not the ECG. Relief of symptomsalways comes first. However, some general pointscan be made about the action that might be takenif the ECG shows conduction abnormalities.

First degree block

∑ Often seen in normal people.∑ Think about acute myocardial infarction

and acute rheumatic fever as possible causes.∑ No specific action needed.

Second degree block

∑ Usually indicates heart disease; often seenin acute myocardial infarction.

∑ Mobitz type 2 and Wenckebach block donot need specific treatment.

∑ 2:1, 3:1 or 4:1 block may indicate a needfor temporary or permanent pacing,especially if the ventricular rate is slow.

Third degree block

∑ Always indicates conducting tissue disease –more often fibrosis than ischaemic.

∑ Consider a temporary or permanentpacemaker.

Right bundle branch block

∑ Think about an atrial septal defect. ∑ No specific treatment.

Left bundle branch block

∑ Think about aortic stenosis and ischaemicdisease.

∑ If the patient is asymptomatic, no action isneeded.

∑ If the patient has recently had severe chestpain, LBBB may indicate an acute myocardialinfarction, and intervention should beconsidered.

Left axis deviation

∑ Think about left ventricular hypertrophyand its causes.

∑ No action needed.

Left axis deviation and right bundlebranch block

∑ Indicates severe conducting tissue disease.∑ No specific treatment needed.∑ Pacemaker required if the patient has

symptoms suggestive of intermittentcomplete heart block.

2Reminders

55

REMINDERS

CONDUCTION AND ITS EFFECTS ON THE ECG

∑ The ECG pattern of RBBB and LBBB can beworked out if you remember that:

– the septum is depolarized first from leftto right

– lead V1 looks at the right ventricle andlead V6 at the left ventricle

– when depolarization spreads towardsan electrode the stylus moves upwards.

∑ If you can’t remember all this, rememberthat RBBB has an RSR1 pattern in lead V1, while LBBB has a letter ‘M’ pattern inlead V6.

∑ Block of the anterior division or fascicle of the left bundle branch causes left axisdeviation.

∑ Depolarization normally begins in the SAnode, and spreads to the ventricles via theAV node, the His bundle, the right and leftbranches of the His bundle, and the anteriorand posterior fascicles of the left bundlebranch.

∑ A conduction abnormality can develop atany of these points.

∑ Conduction problems in the AV node andHis bundle may be partial (first and seconddegree block) or complete (third degreeblock).

∑ If conduction is normal through the AV node, the His bundle and one of itsbranches, but is abnormal in the otherbranch, bundle branch block exists and the QRS complex is wide.

ECGIP

For more on

treatment of

conduction

problems with

pacemakers, see

pp. 187–206

ECGIP

For more on

conduction

problems, see

pp. 85–95

56

The rhythm of the heart

The intrinsic rhythmicity of the heart 57

Abnormal rhythms 58

The bradycardias – the slow rhythms 59

Extrasystoles 63

The tachycardias – the fast rhythms 66

Fibrillation 76

The Wolff–Parkinson–White (WPW)

syndrome 79

The origins of tachycardias 81

What to do 82

The identification of rhythm abnormalities 83

So far we have only considered the spread ofdepolarization that follows the normal activationof the sinoatrial (SA) node. When depolarizationbegins in the SA node the heart is said to be insinus rhythm. Depolarization can, however, begin

in other places. Then the rhythm is named afterthe part of the heart where the depolarizationsequence originates, and an ‘arrhythmia’ is saidto be present.

When attempting to analyse a cardiac rhythmremember:

∑ Atrial contraction is associated with the Pwave of the ECG.

∑ Ventricular contraction is associated withthe QRS complex.

∑ Atrial contraction normally precedesventricular contraction, and there is normallyone atrial contraction per ventricularcontraction (i.e. there should be as many P waves as there are QRS complexes).

The keys to rhythm abnormalities are:

∑ The P waves – can you find them? Look forthe lead in which they are most obvious.

∑ The relationship between the P waves andthe QRS complexes – there should be one P wave per QRS complex.

3

∑ The width of the QRS complexes (shouldbe 120 ms or less).

∑ Because an arrhythmia should be identifiedfrom the lead in which the P waves can be seen most easily, full 12-lead ECGs arebetter than rhythm strips.

THE INTRINSIC RHYTHMICITY OF

THE HEART

Most parts of the heart can depolarizespontaneously and rhythmically, and the rate ofcontraction of the ventricles will be controlledby the part of the heart that is depolarizingmost frequently.

The stars in the figures in this chapter indicatethe part of the heart where the activation

sequence began. The SA node normally has thehighest frequency of discharge. Therefore therate of contraction of the ventricles will equalthe rate of discharge of the SA node. The rateof discharge of the SA node is influenced by thevagus nerves, and also by reflexes originating inthe lungs. Changes in heart rate associated withrespiration are normally seen in young people,and this is called ‘sinus arrhythmia’ (Fig. 3.1).

A slow sinus rhythm (‘sinus bradycardia’)can be associated with athletic training, faintingattacks, hypothermia or myxoedema, and isalso often seen immediately after a heart attack.A fast sinus rhythm (‘sinus tachycardia’) can beassociated with exercise, fear, pain, haemorrhageor thyrotoxicosis. There is no particular ratethat is called ‘bradycardia’ or ‘tachycardia’ –these are merely descriptive terms.

3The intrinsic rhythmicity of the heart

57

Sinus arrhythmia

Fig. 3.1

Note

∑ One P wave per QRS complex

∑ Constant PR interval

∑ Progressive beat-to-beat change in

the R–R interval

ABNORMAL RHYTHMS

Abnormal cardiac rhythms can begin in one of three places (Fig. 3.2): the atrial muscle; the region around the atrioventricular (AV)node (this is called ‘nodal’ or, more properly,junctional’); or the ventricular muscle. Although

Figure 3.2 suggests that electrical activationmight begin at specific points within the atrialand ventricular muscles, abnormal rhythms canbegin anywhere within the atria or ventricles.

Sinus rhythm, atrial rhythm and junctionalrhythm together constitute the ‘supraventricular’rhythms (Fig. 3.3). In the supraventricular

58


Division of abnormal rhythms into supraventricular and ventricular

Fig. 3.3

Supraventricular

Ventricular

Points where cardiac rhythms can begin

Fig. 3.2

SA node

Atrial muscle

AV node

Ventricular muscle

the SA node, the atrial muscle, or thejunctional region.

In ventricular rhythms, on the other hand,the depolarization wave spreads through theventricles by an abnormal and slower pathway,via the Purkinje fibres (Fig. 3.5). The QRScomplex is therefore wide and is abnormallyshaped. Repolarization is also abnormal, so theT wave is also of abnormal shape.

Remember:

∑ Supraventricular rhythms have narrowQRS complexes.

∑ Ventricular rhythms have wide QRScomplexes.

∑ The only exception to this rule occurswhen there is a supraventricular rhythmwith right or left bundle branch block, or the Wolff–Parkinson–White (WPW)syndrome, when the QRS complex will be wide (see p. 79).

Abnormal rhythms arising in the atrialmuscle, the junctional region or the ventricularmuscle can be categorized as:

∑ bradycardias – slow and sustained∑ extrasystoles – occur as early single beats∑ tachycardias – fast and sustained∑ fibrillation – activation of the atria or

ventricles is totally disorganized.

THE BRADYCARDIAS – THE SLOW

RHYTHMS

It is clearly advantageous if different parts ofthe heart are able to initiate the depolarization

3The bradycardias – the slow rhythms

59

rhythms, the depolarization wave spreads tothe ventricles in the normal way via the Hisbundle and its branches (Fig. 3.4). The QRScomplex is therefore normal, and is the samewhether depolarization was initiated by

Spread of the depolarization wave in

supraventricular rhythms

Fig. 3.4

Spread of the depolarization wave in

ventricular rhythm

Fig. 3.5

60


sequence, because this gives the heart a seriesof failsafe mechanisms that will keep it going ifthe SA node fails to depolarize, or if conductionof the depolarization wave is blocked. However,the protective mechanisms must normally beinactive if competition between normal andabnormal sites of spontaneous depolarization isto be avoided. This is achieved by the secondarysites having a lower intrinsic frequency ofdepolarization than the SA node.

The heart is controlled by whichever site isspontaneously depolarizing most frequently:normally this is the SA node, and it gives anormal heart rate of about 70/min. If the SAnode fails to depolarize, control will be assumedby a focus either in the atrial muscle or in theregion around the AV node (the junctionalregion), both of which have spontaneousdepolarization frequencies of about 50/min. Ifthese fail, or if conduction through the Hisbundle is blocked, a ventricular focus will takeover and give a ventricular rate of about 30/min.

These slow and protective rhythms arecalled ‘escape rhythms’, because they occur whensecondary sites for initiating depolarizationescape from their normal inhibition by themore active SA node.

Escape rhythms are not primary disorders,but are the response to problems higher in theconducting pathway. They are commonly seenin the acute phase of a heart attack, when theymay be associated with sinus bradycardia. It isimportant not to try to suppress an escaperhythm, because without it the heart mightstop altogether.

ATRIAL ESCAPE

If the rate of depolarization of the SA nodeslows down and a different focus in the atriumtakes over control of the heart, the rhythm isdescribed as ‘atrial escape’ (Fig. 3.6). Atrialescape beats can occur singly.

NODAL (JUNCTIONAL) ESCAPE

If the region around the AV node takes over asthe focus of depolarization, the rhythm iscalled ‘nodal’, or more properly, ‘junctional’escape (Fig. 3.7).

VENTRICULAR ESCAPE

‘Ventricular escape’ is most commonly seenwhen conduction between the atria andventricles is interrupted by complete heartblock (Fig. 3.8).

Ventricular escape rhythms can occurwithout complete heart block, and ventricularescape beats can be single (Fig. 3.9).

The rhythm of the heart can occasionally becontrolled by a ventricular focus with anintrinsic frequency of discharge faster than thatseen in complete heart block. This rhythm iscalled ‘accelerated idioventricular rhythm’ (Fig.3.10), and is often associated with acutemyocardial infarction. Although the appearanceof the ECG is similar to that of ventriculartachycardia (described later), acceleratedidioventricular rhythm is benign and shouldnot be treated. Ventricular tachycardia shouldnot be diagnosed unless the heart rate exceeds120/min.

3The bradycardias – the slow rhythms

61

Atrial escape

Fig. 3.6

Note

∑ After one sinus beat the SA node fails

to depolarize

∑ After a delay, an abnormal P wave is

seen because excitation of the atrium

has begun somewhere other than the

SA node

∑ The abnormal P wave is followed by a

normal QRS complex, because

excitation has spread normally down

the His bundle

∑ The remaining beats show a return to

sinus arrhythmia

Nodal (junctional) escape

Fig. 3.7

Note


∑ Junctional escape rhythm (following

the arrow), rate 75/min

∑ No P waves in junctional beats

(indicates either no atrial contraction

or P wave lost in QRS complex)


62


P QRS

Complete heart block

Fig. 3.8

Note

∑ Regular P waves (normal atrial

depolarization)

∑ P wave rate 145/min

∑ QRS complexes highly abnormal

because of abnormal conduction

through ventricular muscle

∑ QRS complex (ventricular escape) rate

15/min

∑ No relationship between P waves and

QRS complexes

Ventricular escape

Fig. 3.9

Note

∑ After three sinus beats, the SA node

fails to discharge

∑ No atrial or nodal escape occurs

∑ After a pause there is a single wide

and abnormal QRS complex

(arrowed), with an abnormal T wave

∑ A ventricular focus controls the heart

for one beat, and sinus rhythm is then

restored

3Extrasystoles

63

EXTRASYSTOLES

Any part of the heart can depolarize earlier thanit should, and the accompanying heartbeat iscalled an extrasystole. The term ‘ectopic’ issometimes used to indicate that depolarizationoriginated in an abnormal location, and the term‘premature contraction’ means the same thing.

The ECG appearance of an extrasystolearising in the atrial muscle, the junctional ornodal region, or the ventricular muscle, is thesame as that of the corresponding escape beat –the difference is that an extrasystole comes earlyand an escape beat comes late.

Atrial extrasystoles have abnormal P waves(Fig. 3.11). In a junctional extrasystole there is

Accelerated idioventricular rhythm

Fig. 3.10

Note

∑ After three sinus beats, the SA node

fails to depolarize

∑ An escape focus in the ventricle

takes over, causing a regular rhythm

of 75/min with wide QRS complexes

and abnormal T waves

Sinus Atrial

Junctional

Atrial and junctional (nodal) extrasystoles

Fig. 3.11

Note

∑ This record shows sinus rhythm with

junctional and atrial extrasystoles

∑ A junctional extrasystole has no P wave

∑ An atrial extrasystole has an

abnormally shaped P wave

∑ Sinus, junctional and atrial beats have

identical QRS complexes – conduction

in and beyond the His bundle is normal

no P wave at all, or the P wave appearsimmediately before or immediately after theQRS complex (Fig. 3.11). The QRS complexesof atrial and junctional extrasystoles are, ofcourse, the same as those of sinus rhythm.

Ventricular extrasystoles, however, haveabnormal QRS complexes, which are typicallywide and can be of almost any shape (Fig. 3.12).

Ventricular extrasystoles are common, and areusually of no importance. However, when theyoccur early in the T wave of a preceding beatthey can induce ventricular fibrillation (see p. 79),and are thus potentially dangerous.

It may, however, not be as easy as this,particularly if a beat of supraventricular originis conducted abnormally to the ventricles

64


R on T phenomenon:

Ventricular extrasystole

Fig. 3.12

Note

∑ The upper trace shows five sinus

beats, then an early beat with a wide

QRS complex and an abnormal T

wave: this is a ventricular extrasystole

(arrowed)

∑ In the lower trace, the ventricular

extrasystoles occur (arrowed) at the

peak of the T waves of the preceding

sinus beats: this is the ‘R on T’

phenomenon

3Extrasystoles

65

(bundle branch block, see Ch. 2). It is advisableto get into the habit of asking five questionsevery time an ECG is being analysed:

1. Does an early QRS complex follow an earlyP wave? If so, it must be an atrial extrasystole.

2. Can a P wave be seen anywhere? A junctionalextrasystole may cause the appearance of aP wave very close to, and even after, the QRScomplex because excitation is conductedboth to the atria and to the ventricles.

3. Is the QRS complex the same shapethroughout (i.e. has it the same initialdirection of deflection as the normal beat, and has it the same duration)?Supraventricular beats look the same as each other; ventricular beats may lookdifferent from each other.

4. Is the T wave the same way up as in thenormal beat? In supraventricular beats, it is the same way up; in ventricular beats, it is inverted.

5. Does the next P wave after the extrasystoleappear at an expected time? In bothsupraventricular and ventricular extrasystolesthere is a (‘compensatory’) pause before the next heartbeat, but a supraventricularextrasystole usually upsets the normalperiodicity of the SA node, so that the nextSA node discharge (and P wave) comes late.

The effects of both supraventricular andventricular extrasystoles on the following P waveare as follows:

∑ A supraventricular extrasystole resets the P wave cycle (Fig. 3.13).

No P wave

Expected P waveP

Supraventricular extrasystole

Fig. 3.13

Note

∑ Three sinus beats are followed by a

junctional extrasystole

∑ No P wave is seen at the expected

time, and the next P wave is late

∑ A ventricular extrasystole, on the otherhand, does not affect the SA node, so thenext P wave appears at the predicted time(Fig. 3.14).

THE TACHYCARDIAS – THE FAST

RHYTHMS

Foci in the atria, the junctional (AV nodal) region,and the ventricles may depolarize repeatedly,causing a sustained tachycardia. The criteriaalready described can be used to decide theorigin of the arrhythmia, and as before the mostimportant thing is to try to identify a P wave.When a tachycardia occurs intermittently, it is

called ‘paroxysmal’: this is a clinical description,and is not related to any specific ECG pattern.

SUPRAVENTRICULAR TACHYCARDIAS

Atrial tachycardia (abnormal focus in theatrium)

In atrial tachycardia, the atria depolarize fasterthan 150/min (Fig. 3.15).

The AV node cannot conduct atrial rates of discharge greater than about 200/min. If theatrial rate is faster than this, ‘atrioventricularblock’ occurs, with some P waves not followedby QRS complexes. The difference between thissort of atrioventricular block and second degreeheart block is that in atrioventricular block

66


No P wave

Expected P waveP

Ventricular extrasystole

Fig. 3.14

Note

∑ Three sinus beats are followed by a

ventricular extrasystole

∑ No P wave is seen after this beat, but

the next P wave arrives on time

associated with tachycardia the AV node isfunctioning properly – it is preventing theventricles from being activated at a fast (andtherefore inefficient) rate. In first, second orthird degree block associated with sinus rhythm,the AV node and/or the His bundle are notconducting normally.

Atrial flutter

When the atrial rate is greater than 250/min,and there is no flat baseline between the Pwaves, ‘atrial flutter’ is present (Fig. 3.16).

When atrial tachycardia or atrial flutter isassociated with 2:1 block, you need to lookcarefully to recognize the extra P waves (Fig.3.17). A narrow complex tachycardia with aventricular rate of about 125–150/min shouldalways alert you to the possibility of atrialflutter with 2:1 block.

Any arrhythmia should be identified fromthe lead in which P waves can most easily beseen. In the record in Figure 3.18, atrial flutteris most easily seen in lead II, but it is alsoobvious in leads VR and VF.

3The tachycardias – the fast rhythms

67

Atrial tachycardia

Fig. 3.15

Note

∑ After three sinus beats, atrial

tachycardia develops at a rate of

150/min

∑ P waves can be seen superimposed

on the T waves of the preceding

beats

∑ The QRS complexes have the same

shape as those of the sinus beats

68


P

Atrial flutter

Fig. 3.16

Note

∑ P waves can be seen at a rate

of 300/min, giving a ‘sawtooth’

appearance

∑ There are four P waves per QRS

complex (arrowed)

∑ Ventricular activation is perfectly

regular at 75/min

P

Atrial flutter with 2:1 block

Fig. 3.17

Note

∑ Atrial flutter with an atrial rate of

250/min is present, and there is 2:1

block, giving a ventricular rate of

125/min

∑ The first of the two P waves associated

with each QRS complex can be

mistaken for the T wave of the

preceding beat, but P waves can

be identified by their regularity

∑ In this trace, T waves cannot be

clearly identified

V1 V4VRI

V2 V5VLII

V3 V6VFIII


69

Fig. 3.18

Atrial flutter with 2:1 blockNote

∑ P waves at just over 300/min (most easily seen in leads II and VR)

∑ Regular QRS complexes, rate 160/min

∑ Narrow QRS complexes of normal shape

∑ Normal T waves (best seen in the V leads; in the limb leads it is difficult to distinguish between T and

P waves)

70


Sinus rhythm:

Junctional tachycardia:

Junctional (nodal) tachycardia

Fig. 3.19

Note

∑ In the upper trace there are no P

waves, and the QRS complexes are

completely regular

∑ The lower trace is from the same

patient, in sinus rhythm. The QRS

complexes have essentially the same

shape as those of the junctional

tachycardia

Junctional (nodal) tachycardia

If the area around the AV node depolarizesfrequently, the P waves may be seen very closeto the QRS complexes, or may not be seen atall (Fig. 3.19). The QRS complex is of normalshape because, as with the other supraventricular

arrhythmias, the ventricles are activated via theHis bundle in the normal way.

The 12-lead ECG in Figure 3.20 shows thatin junctional tachycardia no P waves can beseen in any lead.

V1 V4VRI

V2 V5VLII

V3 V6VFIII


71

Fig. 3.20

Junctional tachycardiaNote

∑ No P waves



∑ Normal T waves

72


CSP

Atrial flutter with carotid sinus pressure (CSP)

Fig. 3.21

Note

∑ In this case, carotid sinus pressure

(applied during the period indicated

by the arrows) has increased the block

between the atria and the ventricles,

and has made it obvious that the

underlying rhythm is atrial flutter

Carotid sinus pressure

Carotid sinus pressure may have a usefultherapeutic effect on supraventricular tachycardias,and is always worth trying because it may makethe nature of the arrhythmia more obvious(Fig. 3.21). Carotid sinus pressure activates areflex that leads to vagal stimulation of the SAand AV nodes. This causes a reduction in the

frequency of discharge of the SA node, and anincrease in the delay of conduction in the AVnode. It is the latter which is important in thediagnosis and treatment of arrhythmias. Carotidsinus pressure completely abolishes somesupraventricular arrhythmias, and slows theventricular rate in others, but it has no effecton ventricular arrhythmias.


VENTRICULAR TACHYCARDIAS

If a focus in the ventricular muscle depolarizeswith a high frequency (causing, in effect, rapidlyrepeated ventricular extrasystoles), the rhythmis called ‘ventricular tachycardia’ (Fig. 3.22).

Excitation has to spread by an abnormalpath through the ventricular muscle, and theQRS complex is therefore wide and abnormal.

Wide and abnormal complexes are seen in all12 leads of the standard ECG (Fig. 3.23).

Remember that wide and abnormalcomplexes are also seen with bundle branchblock (Fig. 3.24).

73

Ventricular tachycardia

Fig. 3.22

Note

∑ After two sinus beats, the rate

increases to 200/min

∑ The QRS complexes become broad,

and the T waves are difficult to

identify

∑ The final beat shows a return to sinus

rhythm

ECGIP

For more on

broad complex

tachycardias,

see p. 126

74


VRI

VLII

VFIII

V1 V4

V2 V5

V3 V6

Fig. 3.23

Ventricular tachycardiaNote

∑ No P waves


∑ Broad QRS complexes, duration 280 ms, with a very abnormal shape

∑ No identifiable T waves


HOW TO DISTINGUISH BETWEENVENTRICULAR TACHYCARDIA ANDSUPRAVENTRICULAR TACHYCARDIA WITH BUNDLE BRANCH BLOCK

It is essential to remember that the patient’sclinical state – whether good or bad – does nothelp to differentiate between the two possiblecauses of a tachycardia with broad QRScomplexes. If a patient with an acute myocardialinfarction has broad complex tachycardia itwill almost always be ventricular tachycardia.However, a patient with episodes of broadcomplex tachycardia but without an infarction

could have ventricular tachycardia, orsupraventricular tachycardia with bundle branchblock or the Wolff–Parkinson–White syndrome(see p. 79). Under such circumstances thefollowing points may be helpful:

1. Finding P waves and seeing how they relateto the QRS complexes is always the key to identifying arrhythmias. Always lookcarefully at a full 12-lead ECG.

2. If possible, compare the QRS complexduring the tachycardia with that duringsinus rhythm. If the patient has bundlebranch block when in sinus rhythm, the

75

Sinus rhythm with left bundle branch block

Fig. 3.24

Note

∑ Sinus rhythm: each QRS complex is

preceded by a P wave, with a constant

PR interval

∑ The QRS complexes are wide and the

T waves are inverted

∑ This trace was recorded from lead

V6, and the M pattern and inverted

T wave characteristic of left bundle

branch block are easily identifiable

QRS complex during the tachycardia willhave the same shape as during normalrhythm.

3. If the QRS complex is wider than foursmall squares (160 ms), the rhythm willprobably be ventricular in origin.

4. Left axis deviation during the tachycardiausually indicates a ventricular origin, asdoes any change of axis compared with arecord taken during sinus rhythm.

5. If during the tachycardia the QRS complexis very irregular, the rhythm is probablyatrial fibrillation with bundle branch block(see below).

FIBRILLATION

All the arrhythmias discussed so far haveinvolved the synchronous contraction of all themuscle fibres of the atria or of the ventricles,albeit at abnormal speeds. When individualmuscle fibres contract independently, they are

said to be ‘fibrillating’. Fibrillation can occur inthe atrial or ventricular muscle.

ATRIAL FIBRILLATION

When the atrial muscle fibres contractindependently there are no P waves on theECG, only an irregular line (Fig. 3.25). At timesthere may be flutter-like waves for 2–3 s. TheAV node is continuously bombarded withdepolarization waves of varying strength, anddepolarization spreads at irregular intervalsdown the His bundle. The AV node conductsin an ‘all or none’ fashion, so that thedepolarization waves passing into the Hisbundle are of constant intensity. However, thesewaves are irregular, and the ventricles thereforecontract irregularly. Because conduction into andthrough the ventricles is by the normal route,each QRS complex is of normal shape.

In a 12-lead record, fibrillation waves canoften be seen much better in some leads than inothers (Fig. 3.26).

76


3Fibrillation

77

Lead V1:

Lead II:

Atrial fibrillation

Fig. 3.25

Note

∑ No P waves, and an irregular baseline

∑ Irregular QRS complexes

∑ Normally shaped QRS complexes

∑ In lead V1, waves can be seen with

some resemblance to those seen

in atrial flutter – this is common in

atrial fibrillation

V1 V4VRI

V2 V5VLII

V3 V6VFIII

78


Fig. 3.26

Atrial fibrillationNote

∑ No P waves

∑ Irregular baseline

∑ Irregular QRS complexes, rate varying between 75/min and 190/min


∑ Depressed ST segments in leads V5–V6 (digoxin effect – see p. 101)

∑ Normal T waves

3The Wolff–Parkinson–White (WPW) syndrome

79

VENTRICULAR FIBRILLATION

When the ventricular muscle fibres contractindependently, no QRS complex can beidentified, and the ECG is totally disorganized(Fig. 3.27).

As the patient will usually have lostconsciousness by the time you have realizedthat the change in the ECG pattern is not justdue to a loose connection, the diagnosis is easy.

THE WOLFF–PARKINSON–WHITE

(WPW) SYNDROME

The only normal electrical connection betweenthe atria and ventricles is the His bundle. Some

people, however, have an extra or ‘accessory’conducting bundle, a condition known as theWolff–Parkinson–White syndrome. The accessorybundles form a direct connection between theatrium and the ventricle, usually on the left sideof the heart, and in these bundles there is noAV node to delay conduction. A depolarizationwave therefore reaches the ventricle early, and‘pre-excitation’ occurs. The PR interval is short,and the QRS complex shows an early slurredupstroke called a ‘delta wave’ (Fig. 3.28). Thesecond part of the QRS complex is normal, asconduction through the His bundle catches upwith the pre-excitation. The effects of theWPW syndrome on the ECG are considered inmore detail in Chapter 7.

Ventricular fibrillation

Fig. 3.27

80


I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 3.28

The Wolff–Parkinson–White syndromeNote



∑ Short PR interval

∑ Slurred upstroke of the QRS complex, best seen in leads V3 and V4. Wide QRS

complex due to this ‘delta’ wave

∑ Dominant R wave in lead V1

3The origins of tachycardias

81

Sustained tachycardia in the Wolff–Parkinson–White syndrome

Fig. 3.29

Note

∑ During re-entry tachycardia, no

P waves can be seen

The only clinical importance of thisanatomical abnormality is that it can causeparoxysmal tachycardia. Depolarization canspread down the His bundle and back up theaccessory pathway, and so reactivate the atrium.A ‘re-entry’ circuit is thus set up, and asustained tachycardia occurs (Fig. 3.29).

THE ORIGINS OF TACHYCARDIAS

We have considered the tachycardias up to nowas if all were due to an increased spontaneous

frequency of depolarization of some part of theheart. While such an ‘enhanced automaticity’certainly accounts for some tachycardias, othersare due to re-entry circuits within the heartmuscle. The tachycardias that we havedescribed as ‘junctional’ are usually due tore-entry circuits around the AV node, and aretherefore properly called ‘atrioventricularnodal re-entry tachycardias’ (AVNRTs). It is notpossible to distinguish enhanced automaticityfrom re-entry tachycardia on standard ECGs,but fortunately this differentiation has nopractical importance.

ECGIP

For more

on WPW

syndrome,

see pp. 69–72

WHAT TO DO

Accurate interpretation of the ECG is an essentialpart of arrhythmia management. Although thisbook is not intended to discuss therapy in detail,it seems appropriate to outline some simpleapproaches to patient management that logicallyfollow interpretation of an ECG recording:

1. For fast or slow sinus rhythm, treat theunderlying cause, not the rhythm itself.

2. Extrasystoles rarely need treatment.3. In patients with acute heart failure or low

blood pressure due to tachycardia, DCcardioversion should be considered early on.

4. Patients with any bradycardia that isaffecting the circulation can be treated with atropine, but if this is ineffective theywill need temporary or permanent pacing(Fig. 3.30).

5. The first treatment for any abnormaltachycardia is carotid sinus pressure. This should be performed with the ECGrunning, and may help make the diagnosis:– Sinus tachycardia: carotid sinus pressure

causes temporary slowing of the heartrate.

– Atrial and junctional tachycardia: carotid sinus pressure may terminate the arrhythmia or may have no effect.

– Atrial flutter: carotid sinus pressureusually causes a temporary increase in block (e.g. from 2:1 to 3:1).

– Atrial fibrillation and ventriculartachycardia: carotid sinus pressure has no effect.

6. Narrow complex tachycardias should be treated initially with adenosine.

7. Wide complex tachycardias should be treated initially with lidocaine.

82


Pacemaker

Fig. 3.30

Note

∑ Occasional P waves are visible, but

are not related to the QRS complexes

∑ The QRS complexes are preceded

by a brief spike, representing the

pacemaker stimulus

∑ The QRS complexes are broad, because

pacemakers stimulate the right

ventricle and cause ‘ventricular’ beats

ECGIP

For more on

pacemakers, see

pp. 187–207

3The identification of rhythm abnormalities

83

THE IDENTIFICATION OF RHYTHM

ABNORMALITIES

Recognizing ECG abnormalities is to a largeextent like recognizing an elephant – once seen,never forgotten. However, in cases of difficultyit is helpful to ask the following questions,referring to Table 3.1:

1. Is the abnormality occasional or sustained?2. Are there any P waves?3. Are there as many QRS complexes as

P waves?4. Are the ventricles contracting regularly

or irregularly?5. Is the QRS complex of normal shape?6. What is the ventricular rate?

REMINDERS

ABNORMAL CARDIAC RHYTHMS

∑ Apart from the rate, the ECG patterns of an escape rhythm, an extrasystole and atachycardia arising in any one part of theheart are the same.

∑ All supraventricular rhythms have normalQRS complexes, provided there is nobundle branch block or pre-excitation(WPW) syndrome.

∑ Ventricular rhythms cause wide andabnormal QRS complexes, and abnormal T waves.

∑ Most parts of the heart are capable ofspontaneous depolarization.

∑ Abnormal rhythms can arise in the atrialmuscle, the region around the AV node (the junctional region) and in the ventricular muscle.

∑ Escape rhythms are slow and areprotective.

∑ Occasional early depolarization of any part of the heart causes an extrasystole.

∑ Frequent depolarization of any part of theheart causes tachycardia.

∑ Asynchronous contraction of muscle fibres in the atria or ventricles is called fibrillation.

ECGIP

For more on

tachycardias,

see pp. 113–147

Table 3.1 Recognizing ECG abnormalities

Abnormality P wave P:QRS ratio QRS regularity QRS shape QRS rate Rhythm

Occasional Normal Supraventricular

(i.e. extrasystoles)Abnormal Ventricular

Sustained Present P:QRS = 1:1 Regular Normal Normal Sinus rhythm

≥150/min Atrial tachycardia

Slightly irregular Normal Normal Sinus arrhythmia

Slow Atrial escape

More P waves Regular Normal Fast Atrial tachycardia

than QRS with blockcomplexes

Slow Second degree

heart block

Abnormal Slow Complete heart

block

Absent Regular Normal Fast Junctional

tachycardia

Slow Junctional

escape

Abnormal Fast Junctional

tachycardia

n/a with bundle

branch block

or ventricular

tachycardia

Irregular Normal Any speed Atrial fibrillation

Abnormal Any speed Atrial fibrillation

and bundle

branch block

QRS complexes Ventricular

absent fibrillation or

standstill

84


85

4Abnormalities of P waves,QRS complexes and T waves

Abnormalities of the P wave 86

Abnormalities of the QRS complex 87

Abnormalities of the ST segment 96

Abnormalities of the T wave 98

Other abnormalities of the ST segment

and the T wave 101

When interpreting an ECG, identify the rhythmfirst. Then ask the following questions – alwaysin the same sequence:

1. Are there any abnormalities of the P wave?2. What is the direction of the cardiac axis?

(Look at the QRS complex in leads I, IIand III – and at Ch. 1 if necessary.)

3. Is the QRS complex of normal duration?4. Are there any abnormalities in the QRS

complex – particularly, are there anyabnormal Q waves?

5. Is the ST segment raised or depressed?6. Is the T wave normal?

Remember:

1. The P wave can only be normal, unusuallytall or unusually broad.

2. The QRS complex can only have threeabnormalities – it can be too broad or too tall, and it may contain an abnormal Q wave.

3. The ST segment can only be normal,elevated or depressed.

4. The T wave can only be the right way up or the wrong way up.

86

Abnormalities of P waves, QRS complexes and T waves

Right atrial hypertrophy

ABNORMALITIES OF THE P WAVE

Apart from alterations of the shape of the P waveassociated with rhythm changes, there are onlytwo important abnormalities:

1. Anything that causes the right atrium tobecome hypertrophied (such as tricuspid

valve stenosis or pulmonary hypertension)causes the P wave to become peaked (Fig. 4.1).

2. Left atrial hypertrophy (usually due to mitralstenosis) causes a broad and bifid P wave(Fig. 4.2).

Fig. 4.1

Left atrial hypertrophy

Fig. 4.2

4Abnormalities of the QRS complex

87

Right ventricular hypertrophy

Right ventricular hypertrophy is best seen inthe right ventricular leads (especially V1). Sincethe left ventricle does not have its usualdominant effect on the QRS shape, the complexin lead V1 becomes upright (i.e. the height ofthe R wave exceeds the depth of the S wave) –this is nearly always abnormal (Fig. 4.3). Therewill also be a deep S wave in lead V6.

ABNORMALITIES OF THE QRS COMPLEX

The normal QRS complex has fourcharacteristics:

1. Its duration is no greater than 120 ms (threesmall squares).

2. In a right ventricular lead (V1), the S waveis greater than the R wave.

3. In a left ventricular lead (V5 or V6), theheight of the R wave is less than 25 mm.

4. Left ventricular leads may show Q waves dueto septal depolarization, but these are lessthan 1 mm across and less than 2 mm deep.

ABNORMALITIES OF THE WIDTH OF THEQRS COMPLEX

QRS complexes are abnormally wide in thepresence of bundle branch block (see Ch. 2), orwhen depolarization is initiated by a focus inthe ventricular muscle causing ventricularescape beats, extrasystoles or tachycardia (seeCh. 3). In each case, the increased widthindicates that depolarization has spreadthrough the ventricles by an abnormal andtherefore slow pathway. The QRS complex isalso wide in the Wolff–Parkinson–Whitesyndrome (see p. 79, Ch. 3).

INCREASED HEIGHT OF THE QRS COMPLEX

An increase of muscle mass in either ventriclewill lead to increased electrical activity, and toan increase in the height of the QRS complex.

The QRS complex in right ventricular

hypertrophy

Fig. 4.3

S

R

V6

V1

88


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Right ventricular hypertrophy is usuallyaccompanied by right axis deviation (see Ch.1), by a peaked P wave (right atrial hypertrophy),

and in severe cases by inversion of the T wavesin leads V1 and V2, and sometimes in lead V3or even V4 (Fig. 4.4).

Fig. 4.4

Severe right ventricular hypertrophyNote


∑ Right axis deviation (deep S waves in lead I)

∑ Dominant R waves in lead V1

∑ Deep S waves in lead V (clockwise rotation)

∑ Inverted T waves in leads II, III, VF and V1–V3

∑ Flat T waves in leads V4–V5


89

Pulmonary embolism

In pulmonary embolism the ECG may showfeatures of right ventricular hypertrophy (Fig.4.5), although in many cases there is nothingabnormal other than sinus tachycardia. When apulmonary embolus is suspected, look for anyof the following:

1. Peaked P waves.2. Right axis deviation (S waves in lead I).3. Tall R waves in lead V1.4. Right bundle branch block.5. Inverted T waves in lead V1 (normal),

spreading across to lead V2 or V3.6. A shift of transition point to the left,

so that the R wave equals the S wave

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 4.5

Pulmonary embolismNote



∑ Peaked P waves, especially in lead II

∑ Persistent S wave in lead V6

∑ T wave inversion in leads V1–V4

90


in lead V5 or V6 rather than in lead V3 orV4 (clockwise rotation). A deep S wave willpersist in lead V6.

7. Curiously, a ‘Q’ wave in lead III resemblingan inferior infarction (see below).

However, do not hesitate to treat the patient ifthe clinical picture suggests pulmonary embolismbut the ECG does not show the classical pattern

of right ventricular hypertrophy. If in doubt,treat the patient with an anticoagulant.

Left ventricular hypertrophy

Left ventricular hypertrophy causes a tall Rwave (greater than 25 mm) in lead V5 or V6and a deep S wave in lead V1 or V2 (Fig. 4.6) –but in practice such ‘voltage’ changes alone are

I VR V1 V4

II VL V2 V5

III VFV3 V6

Fig. 4.6

Left ventricular hypertrophyNote


∑ Normal axis

∑ Tall R waves in leads V5–V6 (R wave in lead V5, 40 mm) and deep S waves in leads V1–V2

∑ Inverted T waves in leads I, VL and V5–V6


91

unhelpful in diagnosing left ventricularenlargement. With significant hypertrophy,there are also inverted T waves in leads I, VL,V5 and V6, and sometimes V4, and there may beleft axis deviation. It is difficult to diagnoseminor degrees of left ventricular hypertrophyfrom the ECG.

THE ORIGIN OF Q WAVES

Small (septal) ‘Q’ waves in the left ventricularleads result from depolarization of the septumfrom left to right (see Ch. 1). However, Qwaves greater than one small square in width(representing 40 ms) and greater than 2 mm indepth have a quite different significance.

The ventricles are depolarized from insideoutwards (Fig. 4.7). Therefore, an electrodeplaced in the cavity of a ventricle would recordonly a Q wave, because all the depolarizationwaves would be moving away from it. If amyocardial infarction causes complete death ofmuscle from the inside surface to the outsidesurface of the heart, an electrical ‘window’ iscreated, and an electrode looking at the heartover that window will record a cavity potential –that is, a Q wave.

Q waves greater than one small square inwidth and at least 2 mm deep therefore indicatea myocardial infarction, and the leads in whichthe Q wave appears give some indication of thepart of the heart that has been damaged. Thus,infarction of the anterior wall of the leftventricle causes a Q wave in the leads looking

at the heart from the front – V2–V4 or V5 (Fig.4.8) (see Ch. 1).

If the infarction involves both the anteriorand lateral surfaces of the heart, a Q wave willbe present in leads V3 and V4 and in the leadsthat look at the lateral surface – I, VL andV5–V6 (Fig. 4.9).

Infarctions of the inferior surface of the heartcause Q waves in the leads looking at the heartfrom below – III and VF (Figs 4.8 and 4.10).

When the posterior wall of the left ventricle isinfarcted, a different pattern is seen (Fig. 4.11).The right ventricle occupies the front of theheart anatomically, and normally depolarizationof the right ventricle (moving towards therecording electrode V1) is overshadowed bydepolarization of the left ventricle (moving awayfrom V1). The result is a dominant S wave in leadV1. With infarction of the posterior wall of the

The origin of Q waves

Fig. 4.7

V6

Q

92


left ventricle, depolarization of the right ventricleis less opposed by left ventricular forces, and sobecomes more obvious, and a dominant R wavedevelops in lead V1. The appearance of the ECGis similar to that of right ventricular hypertrophy,

though the other changes of right ventricularhypertrophy (see above) do not appear.

The presence of a Q wave does not give anyindication of the age of an infarction, because oncea Q wave has developed it is usually permanent.

VRI

VLII

VFIII

V1 V4

V2 V5

V3 V6

Fig. 4.8

Acute anterior myocardial infarction, and probable old inferior infarctionNote


∑ Normal axis

∑ Small Q waves in leads II, III and VF – associated with flat ST segments and inverted T waves – indicate old

inferior infarction

∑ Small Q waves in leads V3–V4 – associated with raised ST segments – indicate acute anterior infarction

ECGIP

For more on

myocardial

infarction, see

pp. 214–241


93

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 4.9

Acute anterolateral myocardial infarction and left anterior hemiblockNote


∑ Left axis deviation (dominant S waves in leads II and III)

∑ Q waves in leads VL and V2–V3

∑ Raised ST segments in leads I, VL and V2–V5

94


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 4.10

Acute inferior infarction; lateral ischaemiaNote


∑ Normal axis

∑ Q waves in leads III and VF


∑ Raised ST segments in leads II, III and VF

∑ Inverted T waves in lead VL (abnormal) and in lead V1 (normal)


95

VRI

VLII

VFIII

V1 V4

V2 V5

V3 V6

Fig. 4.11

Posterior myocardial infarctionNote


∑ Normal axis

∑ Dominant R waves in lead V1

∑ Flattened T waves in leads I and VL

96


ABNORMALITIES OF THE ST SEGMENT

The ST segment lies between the QRS complexand the T wave (Fig. 4.12). It should be‘isoelectric’ – that is, at the same level as the partbetween the T wave and the next P wave – but

The ST segment

Fig. 4.12

ST segment

(a) Elevated ST segment. (b) Depressed ST segment

Fig. 4.13

(a) (b)

it may be elevated (Fig. 4.13a) or depressed(Fig. 4.13b).

Elevation of the ST segment is an indicationof acute myocardial injury, usually due either toa recent infarction or to pericarditis. The leadsin which the elevation occurs indicate the part

4Abnormalities of the ST segment

97

of the heart that is damaged – anterior damageshows in the V leads, and inferior damage inleads III and VF (see Figs 4.8 and 4.10).Pericarditis is not usually a localized affair, andso it causes ST elevation in most leads.

Horizontal depression of the ST segment,associated with an upright T wave, is usually a

sign of ischaemia as opposed to infarction. Whenthe ECG at rest is normal, ST segment depressionmay appear during exercise, particularly wheneffort induces angina (Fig. 4.14).

Downward-sloping – as opposed to horizontallydepressed – ST segments are usually due totreatment with digoxin (see p. 101).

Exercise-induced ischaemic changes

Fig. 4.14

Exercise:

Rest:

Note

∑ In the upper (normal) trace, the heart

rate is 55/min and the ST segments

are isoelectric

∑ In the lower trace, the heart rate is

125/min and the ST segments are

horizontally depressed

98


ABNORMALITIES OF THE T WAVE

INVERSION OF THE T WAVE

The T wave is normally inverted in leads VRand V1, sometimes in leads III and V2, and alsoin lead V3 in some black people.

T wave inversion is seen in the followingcircumstances:

1. Normality2. Ischaemia3. Ventricular hypertrophy4. Bundle branch block5. Digoxin treatment.

Leads adjacent to those showing inverted T waves sometimes show ‘biphasic’ T waves –initially upright and then inverted.

MYOCARDIAL INFARCTION

After a myocardial infarction, the first abnormalityseen on the ECG is elevation of the ST segment(Fig. 4.15). Subsequently, Q waves appear, andthe T waves become inverted. The ST segmentreturns to the baseline, the whole process takinga variable time but usually within the range24–48 h. T wave inversion is often permanent.Infarctions causing this pattern of ECG changesare called ‘ST segment elevation myocardialinfarctions’ (STEMIs) (see p. 130).

If an infarction is not full thickness and sodoes not cause an electrical window, there willbe T wave inversion but no Q waves (Fig. 4.16).Infarctions with this pattern of ECG change arecalled ‘non-ST segment elevation myocardialinfarctions’ (NSTEMIs). The older term for thesame pattern was ‘non-Q wave infarction’ or‘subendocardial infarction’.

VENTRICULAR HYPERTROPHY

Left ventricular hypertrophy causes inverted Twaves in leads looking at the left ventricle (I, II,VL, V5–V6) (see Fig. 4.6). Right ventricularhypertrophy causes T wave inversion in theleads looking at the right ventricle (T waveinversion is normal in lead Vl, and may benormal in lead V2, but in white adults isabnormal in lead V3) (see Fig. 4.4).

BUNDLE BRANCH BLOCK

The abnormal path of depolarization in bundlebranch block is usually associated with anabnormal path of repolarization. Therefore,inverted T waves associated with QRScomplexes which have a duration of 160 ms ormore have no significance in themselves (seeFigs 2.15 and 2.16).

4Abnormalities of the T wave

99

Development of inferior infarction

Fig. 4.15

1 h after onset of pain:

I II III VR VL VF


I II III VR VL VF


I II III VR VL VF

Note

∑ Three ECGs have been recorded over

24 h, and have been arranged

horizontally

∑ Sinus rhythm with a normal cardiac

axis in all three ECGs

∑ The first record is essentially normal

∑ 6 h after the onset of pain, the ST

segments have risen in leads II, III and

VF, and the ST segment is depressed

in leads I, VR and VL. A Q wave has

developed in lead III

∑ 24 h after the onset of pain, a small

Q wave has appeared in lead II, and

more obvious Q waves can be seen

in leads III and VF. The ST segments

have returned to the baseline, and

the T waves are now inverted in leads

III and VF

100


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 4.16

Anterior non-ST segment elevation myocardial infarctionNote


∑ Normal axis


∑ Inverted T waves in leads V3–V4

∑ Biphasic T waves in leads V2 and V5

4Other abnormalities of the ST segment and the T wave

101

DIGOXIN

The administration of digoxin causes T waveinversion – characteristically with slopingdepression of the ST segment (Fig. 4.17). It ishelpful to record an ECG before giving digoxin,to save later confusion about the significance ofT wave changes.

OTHER ABNORMALITIES OF THE

ST SEGMENT AND THE T WAVE

ELECTROLYTE ABNORMALITIES

Abnormalities of the plasma levels of potassium,calcium and magnesium affect the ECG, thoughchanges in the plasma sodium level do not. TheT wave and QT interval (measured from theonset of the QRS complex to the end of the Twave) are most commonly affected.

A low potassium level causes T waveflattening and the appearance of a hump on the end of the T wave called a ‘U’ wave. A highpotassium level causes peaked T waves with the disappearance of the ST segment. The QRScomplex may be widened. The effects ofabnormal magnesium levels are similar.

A low plasma calcium level causesprolongation of the QT interval, and a highplasma calcium level shortens it.

NONSPECIFIC CHANGES

Minor degrees of ST segment and T waveabnormalities (T wave flattening, etc.) areusually of no great significance, and are bestreported as ‘nonspecific ST–T changes’.

Digoxin effect

Fig. 4.17

Note

∑ Atrial fibrillation

∑ Narrow QRS complexes

∑ Downward-sloping ST segments

(‘reversed tick’)

∑ Inverted T waves

102


REMINDERS

CAUSES OF ABNORMAL P WAVES, QRS COMPLEXES AND T WAVES

∑ ST segment depression and T waveinversion may be due to ischaemia,ventricular hypertrophy, abnormalintraventricular conduction, or digoxin.

∑ T wave inversion is normal in leads III, VRand V1. T wave inversion is associated withbundle branch block, ischaemia, andventricular hypertrophy.

∑ T wave flattening or peaking with anunusually long or short QT interval may be due to electrolyte abnormalities, butmany minor ST–T changes are nonspecific.

AND REMEMBER

∑ The ECG is easy to understand.

∑ Most abnormalities of the ECG areamenable to reason.

∑ Tall P waves result from right atrialhypertrophy, and broad P waves from left atrial hypertrophy.

∑ Broadening of the QRS complex indicatesabnormal intraventricular conduction: it is seen in bundle branch block and in complexes originating in theventricular muscle. It is also seen in the Wolff–Parkinson–White syndrome.

∑ Increased height of the QRS complexindicates ventricular hypertrophy. Rightventricular hypertrophy is seen in lead V1,and left ventricular hypertrophy is seen in leads V5–V6.

∑ Q waves greater than 1 mm across and2 mm deep indicate myocardial infarction.

∑ ST segment elevation indicates acutemyocardial infarction or pericarditis.

ECGIP

For more on

the effect of

electrolyte

abnormalities,

see pp. 331–334

In practical terms the ECG is simply a tool forthe diagnosis and treatment of patients, andmust always be considered in the light of thepatient’s history and the physical findings.This is because identical ECG appearances –‘normal’ or otherwise – can be seen in healthyand in ill patients.

In this part of the book, we look beyond thebasics and consider how the ECG can help in

103

PartII

the situations in which it is most used – in the‘screening’ of healthy subjects, and in patientswith chest pain, breathlessness, palpitations or syncope. Recalling the classic ECGabnormalities covered in Part I, we will look atsome of the variations that can make ECGinterpretation seem more difficult, usingexamples of more ECGs from patients withcommon problems.

Making the most of the ECGThe clinical interpretation ofindividual ECGs

This page intentionally left blank

The ECG in healthy subjects

The normal cardiac rhythm 105

The P wave 112

Conduction 112

The QRS complex 116

The ST segment 122

The T wave 124

U waves 125

The ECG in athletes 125

The ECG is frequently used in ‘healthscreening’, but it is important to remember thatnot all those who are screened are reallyasymptomatic – the procedure may be used asan alternative to seeking medical advice. Onthe other hand, people being screened may betotally free of symptoms and yet important

abnormalities may be evident from their ECGs.For example, Figure 5.1 shows the ECG of anasymptomatic patient which, quite unexpectedly,revealed atrial fibrillation. Abnormalities areuncommon in this group of individuals, butperhaps are the best reason for using the ECGin screening. All the ECGs in this chapter came from health screening clinics, and we will assume that the individuals consideredthemselves to be healthy.

THE NORMAL CARDIAC RHYTHM

Sinus rhythm is the only truly normal rhythm.‘Sinus bradycardia’ is sometimes said to bepresent when the heart rate is below 60/min,and ‘sinus tachycardia’ is sometimes used forheart rates above 100/min (Box 5.1), but theseterms are really not helpful, and it is far moreuseful to describe a patient as having ‘sinusrhythm at x/min’ (Fig. 5.2).

105

5

V1 V4VRI

V2 V5VLII

V3 V6VFIII

106


Fig. 5.1

Atrial fibrillation in an asymptomatic subjectNote

∑ Atrial fibrillation

∑ Ventricular rate about 85/min

∑ Normal QRS complexes and T waves

∑ There is no ST segment depression, suggesting that the individual is not taking digoxin

5The normal cardiac rhythm

107

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.2

Sinus bradycardia in an athleteNote



Sinus bradycardia

∑ Physical fitness

∑ Vasovagal attacks

∑ Hypothermia

∑ Hypothyroidism

Sinus tachycardia

∑ Exercise, pain, fright

∑ Obesity

∑ Pregnancy

∑ Anaemia

∑ Thyrotoxicosis

∑ CO2 retention

Box 5.1 Causes of sinus bradycardia or tachycardia

108


EXTRASYSTOLES

Supraventricular extrasystoles are of no clinicalsignificance, although atrial extrasystoles needto be differentiated from the variations in beat-to-beat interval which occur in sinus rhythm

(Figs 5.3 and 5.4). Automated ECG reportingoften fails to do this.

Occasional ventricular extrasystoles areexperienced by many people with normal hearts.Frequent ventricular extrasystoles (Fig. 5.5) mayindicate heart disease, and in a large population

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.3

Sinus arrhythmiaNote

∑ Sinus rhythm, rate about 65/min overall

∑ The lead II rhythm strip shows that the rate is initially about 80/min but slows progressively to 60/min

∑ The QRS complexes, ST segments and T waves are normal


109

their presence does identify a group with ahigher than average risk of developing cardiacproblems. In an individual patient, however, theirpresence is not a good predictor of such risk.

Extrasystoles may disappear if alcohol orcoffee intake is reduced, and only need treatingmedically when they are so frequent as toimpair cardiac function.

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.4

Atrial extrasystolesNote

∑ Sinus rhythm; rate as judged from adjacent sinus beats is about 35/min

∑ The overall heart rate, calculated including the extrasystoles, is about 45/min

∑ Extrasystoles are identified by early P waves that are differently shaped compared with those associated

with the sinus beats

∑ The QRS complexes and T waves are the same in the sinus and atrial beats

110


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.5

Ventricular extrasystolesNote


∑ Frequent ventricular extrasystoles, identified by their early occurrence without preceding P waves, and

by their wide and abnormal QRS complex and differently shaped T wave compared with the sinus beats

∑ In the sinus beats the QRS complexes and T waves are normal


111

ECTOPIC ATRIAL RHYTHM

When depolarization is initiated from a focusin the atrium rather than in the sinoatrialnode, an ‘ectopic atrial rhythm’ is present

(Fig. 5.6). This does not cause symptoms andis usually of no clinical significance. It is notan uncommon finding in individuals beingscreened.

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.6

Ectopic atrial rhythmNote

∑ Regular rhythm with inverted P waves in most leads, indicating that an atrial focus controls the heart rate

∑ The PR interval is at the lower end of normal, at 140 ms

∑ Heart rate 60/min

∑ The QRS complexes, ST segments and T waves are all normal

THE P WAVE

Tall P waves may be due to right atrialhypertrophy, and are significant if there isevidence of right ventricular hypertrophy aswell. Tall P waves alone may indicate tricuspidstenosis, but this is rare. If the patient is welland has no abnormal physical signs, ‘tall’ Pwaves are probably within the normal limits.

Bifid P waves in the absence of signs ofassociated left ventricular hypertrophy canindicate mitral stenosis (now fairly rare), but abifid and not particularly prolonged P wave isoften seen in the anterior leads of normal ECGs.Figure 5.7 shows the ECG of an asymptomaticpatient with a clinically normal heart.

The P waves of atrial extrasystoles tend to beabnormally shaped compared to the P waves ofthe sinus beats of the same patient (Fig. 5.4).

P waves cannot always be seen in all leads,but if there is a total absence of P waves therhythm is probably not sinus and may be sinus

arrest, junctional escape or atrial fibrillation; orthe patient may have hyperkalaemia.

CONDUCTION

The upper limit of the PR interval in a normalECG is usually taken as 220 ms, a longer PRinterval indicating first degree heart block.However, the ECGs of healthy individuals,especially athletes, not uncommonly have PRintervals slightly longer than 220 ms, and thesecan be ignored in the absence of any otherindication of heart disease.

The ECG in Figure 5.8 was recorded from ahealthy, asymptomatic individual at a screeningexamination. Nevertheless, PR intervalprolongation to this extent is probably evidenceof disease of the conducting tissue.

Second degree heart block of the Mobitz 1(Wenckebach) type may be seen in athletes, butotherwise second and third degree block areindications of heart disease.

112


ECGIP

For an example

mitral stenosis,

see p. 293

ECGIP

For more on

hyperkalaemia,

see p. 331

5Conduction

113

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.7

Bifid P wavesNote


∑ There are two ventricular extrasystoles

∑ In leads V2, V3 and V4 the P wave is ‘bifid’. This can be a sign of left atrial hypertrophy, but is often seen in

normal ECGs

∑ In the sinus beats the QRS complexes, ST segments and T waves are normal

114


A QRS complex that is predominantlydownward (that is, the S wave is greater thanthe R wave) in leads II and III indicates left axis

deviation, and a downward QRS complex inlead II, still within the normal limit of 120 ms,indicates left anterior hemiblock (Fig. 5.9).

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.8

First degree heart blockNote


∑ PR interval prolonged at 336 ms

∑ Constant PR interval in all beats

∑ Loss of the R wave in lead V3 could indicate an old anterior infarction, otherwise QRS complexes,

ST segments and T waves are normal

5Conduction

115

Right axis deviation is indicated if the QRScomplexes are predominantly downward inlead I. It is common in healthy subjects,particularly if they are tall, as with the ECG inFigure 5.10, and under these circumstances is

unimportant unless there is some otherevidence of right ventricular hypertrophy, orthe patient has had a myocardial infarction,raising the possibility of left posteriorhemiblock.

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.9

Left anterior hemiblockNote


∑ QRS complexes upright in lead I, but mainly downward in leads II and III, indicating left axis deviation

∑ Slightly wide QRS complexes (but still within the normal limit of 120 ms) indicate left anterior hemiblock

∑ QRS complexes and T waves are otherwise normal

116


I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 5.10

Right axis deviationNote


∑ QRS complexes predominantly downward

(S wave greater than R wave) in lead I

THE QRS COMPLEX

Depolarization of the whole ventricular musclemass should occur within 120 ms, so thisrepresents the maximum width of the normalQRS complex. Any widening indicatesconduction delay or failure within the bundlebranch system, pre-excitation (see below), or aventricular origin of depolarization – any ofwhich may be seen in healthy subjects.

Left bundle branch block is always a sign ofheart disease. Right bundle branch block witha QRS complex duration greater than 120 msis sometimes seen in healthy subjects, butshould be taken as a warning of things like anatrial septal defect. Partial (incomplete) rightbundle branch block (RSR1 pattern in lead V1,but with a QRS complex duration less than120 ms; Fig. 5.11) is very common and of nosignificance (Box 5.2).

∑ Upright QRS complexes (R wave greater than

S wave) in leads II–III

∑ QRS complexes and T waves are normal

5The QRS complex

117

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.11

Partial right bundle branch blockNote



∑ RSR1 pattern in lead V1, but the QRS complex duration is normal at 100 ms

∑ QRS complexes, ST segments and T waves are otherwise normal


∑ Normal heart

∑ Atrial septal defect and other congenital disease

∑ Pulmonary embolism


∑ Ischaemia

∑ Aortic stenosis

∑ Hypertension

∑ Cardiomyopathy

Box 5.2 Causes of bundle branch block

118


The height of the QRS complex is related tothe thickness of heart muscle, but is actually apoor indicator of ventricular hypertrophy.

Right ventricular hypertrophy causes adominant R wave in lead V1, but unless thereare other significant ECG signs (right axisdeviation, or T wave inversion in leads V2–V3),this can be a normal variant (Fig. 5.12).

One ECG feature of left ventricularhypertrophy is the increased height of the QRScomplex in the leads that ‘look at’ the leftventricle (Fig. 5.13), the generally acceptedupper limit of normality being a QRS complexheight of 25 mm in lead V5 or V6. TheSokolow–Lyon criteria define left ventricularhypertrophy as being present when the sum of

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.12

Normal ECG with dominant R wave in lead V1

Note


∑ Normal cardiac axis (QRS complexes upright in leads I–III)

∑ Dominant (i.e. predominantly upright) R wave in lead V1

∑ QRS complexes, ST segments and T waves otherwise normal – no other evidence of right ventricular

hypertrophy

5The QRS complex

119

the R wave height in lead V5 or V6 plus thedepth of the S wave in lead V1 exceeds 35 mm.In fact these criteria are unreliable, and a QRScomplex height greater than 25 mm is oftenseen in fit young men. Left ventricularhypertrophy can only be diagnosed withconfidence when tall QRS complexes areassociated with inverted T waves in the lateralleads (see Ch. 4). This is sometimes referred to

as a ‘strain’ pattern, but this term is essentiallymeaningless.

If the QRS complexes seem too small to beconsistent with the clinical findings, check thecalibration of the ECG recorder. If this is correct,possible explanations of small QRS complexesare obesity, emphysema and pericardial effusion.

Q waves are the hallmark of the fullydeveloped changes of an ST segment elevation

V1 V4VRI

V2 V5VLII

V3 V6

VFIII

Fig. 5.13

Normal ECG with increased height of QRS complexes Note



∑ QRS complex: R wave in lead V5 = 45 mm; S wave in lead V1 = 15 mm. This is left ventricular hypertrophy

on voltage criteria, but there is no T wave inversion to suggest significant left ventricular hypertrophy

ECGIP

For more on left

ventricular

hypertrophy,

see pp. 295–302

120


myocardial infarction, but they also result fromseptal depolarization (see p. 17). Narrow Qwaves in the inferior and lateral leads (Fig. 5.14),and sometimes even quite deep ones, may alsobe perfectly normal.

A Q wave in lead III but not in lead VF islikely to be normal, even when associated withan inverted T wave (Fig. 5.15). These featuresoften disappear if the ECG is repeated with thesubject taking and holding in a deep breath.

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.14

Normal ECG with marked infero-lateral Q wavesNote



∑ QRS complexes in leads II, III, VF and V4–V6 show deep but narrow Q waves


∑ Lead V6 shows electrical interference

5The QRS complex

121

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.15

Normal ECG with Q wave and inverted T wave in lead IIINote


∑ The QRS complex in lead III shows a Q wave, and lead VF has a very small Q wave. Otherwise the QRS

complexes are normal

∑ There are inverted T waves in leads III, VR and V1, but not elsewhere

122


THE ST SEGMENT

If the ST segment is raised following an S waveit is described as ‘high take-off ’, and is anormal variant (Fig. 5.16); this pattern istypically seen in the anterior leads. It isimportant to differentiate this from the raised

ST segment of an ST segment elevationmyocardial infarction.

Horizontal ST segment depression is a signof ischaemia (see Ch. 4), but minor degrees ofdepression, often downward-sloping, are seenin the ECGs of normal people, and are bestdescribed as ‘nonspecific’ (Fig. 5.17).

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 5.16

Normal ECG with high take-off ST segments Note


∑ Normal axis


∑ In leads V3–V5 there is a small S wave followed by a small secondary R wave

∑ The ST segment begins 5 mm above the baseline in lead V3, and 2 mm above the baseline in leads V4–V5

5The ST segment

123

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.17

Normal ECG with nonspecific ST segment changesNote


∑ Normal axis


∑ In leads II, III, VF and V5–V6 there is slight downward-sloping ST segment depression

∑ Normal T waves

124


THE T WAVE

The T wave is almost always inverted in leadVR, usually in lead V1 and sometimes in leadIII. Occasionally, a normal heart may beassociated with an inverted T wave in lead V2,and in black people there may be T wave

inversion in leads V3 and V4 as well (Fig. 5.18).This can lead to an incorrect diagnosis of anon-ST segment elevation myocardial infarction(non-Q wave infarction).

Tall and peaked T waves (Fig. 5.19) aresometimes seen in the early stages of amyocardial infarction, when they may be

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 5.18

Normal ECG from a black man Note


∑ Normal axis (there is a dominant S wave in lead III, but a dominant R wave in lead II)

∑ Normal QRS complexes and ST segments

∑ T wave inversion in all the chest leads, especially V2–V5

∑ In a white man this might suggest a non-ST segment elevation myocardial infarction, but in a black man

it is perfectly normal

5The ECG in athletes

125

described as ‘hyperacute’ changes. Peaked Twaves are also associated with hyperkalaemia,but in fact some of the tallest and most peakedT waves are seen in perfectly normal ECGs.

U WAVES

Flat U waves following flat T waves, togetherwith a prolonged QT interval, may be a sign of

hypokalaemia. However, the best examples ofprominent U waves come from normal people(Fig. 5.20).

THE ECG IN ATHLETES

Athletes’ ECGs can show a wide variety ofchanges that could be considered ‘abnormal’(see Box 5.3).

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.19

Normal ECG with marked peaking of the T wavesNote

∑ Sinus rhythm, rate 50/min, with one atrial extrasystole

∑ Normal axis (QRS complexes predominantly

downward in lead III, but upright in leads I and II)

ECGIP

For more on

hypokalaemia,

see pp. 331–334


∑ High take-off ST segments in leads V1–V4

∑ Peaked T waves in leads V2–V4

126


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 5.20

Normal ECG with prominent U wavesNote

∑ The ECG appearance at the beginning is due to

movement of the patient

∑ Sinus rhythm, rate 35/min (sinus bradycardia)

∑ Normal axis

Variations in rhythm

∑ Sinus bradycardia

∑ Junctional rhythm

∑ ‘Wandering’ atrial pacemaker

∑ First degree block

∑ Mobitz type 1 (Wenckebach) second degree block

Box 5.3 Possible ECG features of healthy athletes

Other variations in the ECG

∑ Tall P waves and QRS complexes

∑ Prominent septal Q waves

∑ Counterclockwise rotation

∑ Tall symmetrical T waves

∑ Biphasic T waves

∑ T wave inversion in the lateral leads

∑ Prominent U waves


∑ Peaked T waves in leads V4–V6

∑ Prominent U waves in leads V3–V5

5Reminders

REMINDERS

THE NORMAL ECG

Limits of normal durations

∑ PR interval: 220 ms.

∑ QRS complex duration: 120 ms.

∑ QTc interval: 450 ms.

Rhythm

∑ Sinus arrhythmia.

∑ Supraventricular extrasystoles are alwaysnormal.

The cardiac axis

∑ Normal axis: QRS complexes predominantlyupward in leads I, II and III; still normal if theQRS complex is downward in lead III.

∑ Minor degrees of right and left axisdeviation are within the normal range.

127

QRS complex

∑ Small Q waves are normal in leads I, VL andV6 (septal Q waves).

∑ RSR1 pattern in lead V1 is normal if theduration is less than 120 ms (partial rightbundle branch block).

∑ R wave is smaller than S wave in lead V1.

∑ R wave in lead V6 is less than 25 mm.

∑ R wave in lead V6 plus S wave in lead V1 isless than 35 mm.

ST segment

∑ Should be isoelectric.

T wave

∑ May be inverted in:

– lead III

– lead VR

– lead V1

– leads V2 and V3, in black people.

128

6 The ECG in patients withchest pain or breathlessness

The ECG in patients with constant

chest pain 129

The ECG in patients with intermittent

chest pain 144

The ECG in patients with breathlessness 147

Chest pain is a very common complaint, andwhen reviewing the ECG of a patient withchest pain it is essential to remember that there

are causes other than myocardial ischaemia(Box 6.1).

There are a few features of chest pain thatmake the diagnosis obvious. Chest pain thatradiates to the teeth or jaw is probably cardiacin origin; pain that is worse on inspiration iseither pleuritic or due to pericarditis; and painin the back may be due to either myocardialischaemia or aortic dissection. The ECG willhelp to differentiate these causes of pain but itis not infallible – for example, if an aortic

Acute chest pain

∑ Myocardial infarction

∑ Pulmonary embolism

∑ Pneumothorax and other pleuritic disease

∑ Pericarditis

∑ Aortic dissection

Intermittent chest pain

∑ Angina

∑ Oesophageal pain

∑ Muscular pain

∑ Nonspecific pain

Box 6.1 Causes of chest pain

6The ECG in patients with constant chest pain

129

dissection affects the coronary artery ostia, itcan cause myocardial ischaemia.

THE ECG IN PATIENTS WITH

CONSTANT CHEST PAIN

THE ECG IN ACUTE CORONARYSYNDROMES

‘Acute coronary syndrome’ is a term that coversa spectrum of clinical conditions caused by the rupture of atheromatous plaque within acoronary artery. On the exposed core of theplaque, a thrombus forms, and this can causetotal or partial occlusion of the artery. Theclinical syndrome ranges from angina at rest(unstable angina) to transmural myocardialinfarction, and some definitions of acutecoronary syndrome also include sudden deathdue to coronary occlusion. The diagnosis ofacute coronary syndrome is based on the clinicalpresentation (including a previous history of coronary disease), ECG changes, andbiochemical markers, principally troponin.

If a patient has chest pain and there is ECGevidence of myocardial ischaemia but a normalplasma troponin level, then the diagnosis isacute coronary syndrome due to unstableangina. Myocardial necrosis causes a rise in thelevel of plasma troponin (either troponin T ortroponin I), and a high-sensitivity assay candetect a very small rise. By some definitions,any such rise in a clinical situation suggestingmyocardial ischaemia justifies a diagnosis ofmyocardial infarction. However, the plasma

troponin level may also rise in other conditions,which may also be associated with chest pain(Box 6.2). It is essential to remember that theplasma troponin level may not rise for up to12 h after the onset of chest pain due to amyocardial infarction.

Thus the ECG is an essential tool in thediagnosis of an acute coronary syndrome.Importantly, it also distinguishes between twocategories of myocardial infarction whosemanagement is different. The first is infarctionassociated with ST segment elevation, known as‘ST segment elevation myocardial infarction’ or‘STEMI’, and the second is ‘non-ST segmentelevation myocardial infarction’ or ‘NSTEMI’.Differentiation is important because a STEMIrequires immediate treatment by thrombolysisor percutaneous intervention (PCI – i.e.angioplasty and probably stenting), althoughafter 6 h the benefit of this treatment is largelylost. An NSTEMI may also require PCI but with

∑ Acute pulmonary embolism

∑ Acute pericarditis

∑ Acute or severe heart failure

∑ Sepsis and/or shock

∑ Renal failure

∑ False positive (laboratory problems, including

the presence of heterophilic antibodies and

rheumatoid factor)

Box 6.2 Common causes of plasma troponin level

elevation in the absence of acute myocardial

infarction

of ST segment elevation in at least twocontiguous precordial leads. The diagnosis ofSTEMI can also be accepted if there is leftbundle branch block which is known to be new.

Prompt treatment by PCI or thrombolysismay prevent myocardial damage, so that Qwaves do not develop. Otherwise, after avariable time, usually within a day or so, the STsegments return to the baseline, the T waves inthe affected leads become inverted, and Q wavesdevelop (see p. 91). Once Q waves and invertedT waves have developed following infarction,these ECG changes are usually permanent. Ifanterior ST segment elevation persists, a leftventricular aneurysm should be suspected.

Figures 6.2–6.5 show ECGs from differentpatients with anterior infarctions, at increasingtimes from the onset of symptoms.

An old anterior infarction can also bediagnosed from an ECG that shows a loss of Rwave development in the anterior leads withoutthe presence of Q waves (Fig. 6.6). Thesechanges must be differentiated from those due tochronic lung disease, in which the characteristicchange is a persistent S wave in lead V6. This issometimes called ‘clockwise rotation’ becausethe heart has rotated so that the right ventricleoccupies more of the precordium, and seen frombelow the rotation is clockwise (Fig. 6.7).

130

The ECG in patients with chest pain or breathlessness

considerably less urgency, and the patient isinitially treated with some form of heparin,anti-platelet agents and a beta-blocker.

During the first few hours after the onset ofchest pain due to myocardial infarction theECG can remain apparently normal, and forthis reason ECGs should be recordedrepeatedly in a patient with chest pain thatcould be due to cardiac ischaemia, but whoseECG is nondiagnostic.

UNSTABLE ANGINA

In unstable angina there is ST segmentdepression while the patient has pain (Fig. 6.1).Once the pain has resolved the ECG returns tonormal, or to its previous state if the patienthas had a myocardial infarction in the past.

STEMI

In STEMI the ST segments rise in the ECGleads corresponding to the part of the heartthat is damaged: the V leads with anteriorinfarction, lead VL and the lateral chest leadswith lateral infarction, and leads III and VFwith inferior infarction. STEMI is diagnosedwhen there is more than 1 mm of ST segmentelevation in at least two contiguous limb leads(e.g. I and VL; III and VF), or more than 2 mm


131

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 6.1

ST segment depression in unstable anginaNote


∑ Normal axis


∑ ST segments depressed horizontally in leads V3–V5

∑ Normal T waves

132


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 6.2

ST segment elevation in acute anterior ST segment elevation myocardial infarctionNote


∑ Normal axis


∑ ST segments elevated in leads V1–V5

∑ Normal T waves

∑ The ST segment elevation could be confused with high take-off ST segments, but the trace has to be

interpreted in the context of a patient with acute chest pain


133

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.3

ST segment elevation and Q waves in acute anterior ST segment elevation myocardial

infarctionNote


∑ Left axis deviation (predominantly downward deflection in leads II and III)

∑ Q waves in leads V1–V4

∑ Raised ST segments in leads V2–V4

∑ Inverted T wave in lead VL, and biphasic T wave in lead V3

134


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.4

ST segment elevation and marked Q waves in acute anterior ST segment elevation

myocardial infarctionNote


∑ Normal axis

∑ Deep Q waves and loss of R waves in leads V1–V4

∑ Raised ST segments in leads I, VL and V2–V6


135

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.5

Old anterior ST segment elevation myocardial infarctionNote


∑ Normal axis

∑ Q waves in leads VL and V2–V4

∑ Isoelectric (i.e. at baseline) ST segments (except in lead V4)


136


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.6

Old anterior myocardial infarction with poor R wave progression in the anterior leadsNote


∑ Normal axis (dominant S wave in lead III, but predominantly upright complex in leads I and II)

∑ Isoelectric ST segments

∑ The normal steady progression of R wave development in the anterior leads is missing, with no R wave

in lead V3 but a normal R wave in lead V4

∑ Small Q wave and inverted T wave in lead VL

∑ This pattern might be due to inaccurate placement of the V3 electrode, though the abnormal pattern

in lead VL suggests cardiac disease. The ECG should be repeated


137

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.7

Clockwise rotation in chronic lung diseaseNote


∑ First degree block – PR interval 226 ms

∑ Left anterior hemiblock (predominantly downward complexes in leads II and III)

∑ QRS complexes show a ‘right ventricular’ pattern throughout, with a small R wave and a deep S wave in

lead V6, where there should be a tall R wave and a small S wave

∑ The first degree block and left anterior hemiblock indicate that cardiac disease is present, as well as

chronic lung disease

138


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 6.8

Acute inferior ST segment elevation myocardial infarctionNote


∑ Normal axis

∑ Small Q wave in lead III: other QRS complexes are normal

∑ ST segment elevation of 3 mm in leads II, III and VF

∑ T waves inverted in lead VL

Figures 6.8–6.10 are ECGs from a patientrecorded a few hours after the onset of chestpain and a few days later, and they show thepatterns of inferior infarction. Figure 6.8 shows

a classic inferior STEMI, with, in addition,T wave inversion in lead VL. A few days later(Fig. 6.9), Q waves have appeared in leads IIIand VF, the ST segments have reverted almost


139

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 6.9

Old inferior myocardial infarction (same patient as in Figs 6.8 and 6.9)Note


∑ Normal axis

∑ Q waves in leads III and VF

∑ ST segments in leads II, III and VF have nearly returned to the baseline

∑ T waves inverted in leads II, III and VF

∑ QRS complexes and T waves are normal in the anterior leads

to the baseline, and the T wave in lead VL is nolonger inverted. During the acute phase of aninferior STEMI, conduction disturbances arequite common, as exemplified by the second

degree block in Figure 6.10, showing therhythm strip of an ECG recorded a few hoursafter that shown in Figure 6.8.

140


IIFig. 6.10

Second degree (Wenckebach) heart block in inferior myocardial infarction (same patient as

in Fig. 6.8)Note

∑ Recorded from a monitor lead

∑ Sinus rhythm

∑ Progressive lengthening of the PR interval in the first few beats, followed by a nonconducted P wave, and

then a similar sequence

When an infarction develops in theposterior wall of the left ventricle, Q waves canonly be elicited by placing the chest lead on thepatient’s back. In a routine ECG there will be a dominant R wave in lead V1, caused byunopposed anterior depolarization (Fig. 6.11).

This pattern must be differentiated from thedominant R wave in lead V1 seen in pulmonaryhypertension (see below), and from thedominant R wave that can be a normal variant.Differentiation is best made in the light of thepatient’s history and the physical findings.

ECGIP

For more on

STEMI, see

pp. 214–240


141

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.11

Old posterior myocardial infarctionNote



∑ ST segment depression in leads V1–V3

∑ T wave inversion in leads II, III, VF and V5–V6

∑ This pattern might be confused with a normal variant, or with right ventricular hypertrophy, but the

ST segment and T wave changes suggest ischaemia, and there is no right axis deviation as would be

expected with right ventricular hypertrophy

142


NSTEMI

In NSTEMI there is no ST segment elevation,but there is T wave inversion in the leadscorresponding to the site of myocardial damage(Fig. 6.12). With time the T waves may revertto normal, but inversion may persist. Q wavesdo not develop, and for this reason a distinction

used to be made between ‘Q wave’ and ‘non-Qwave’ infarction. On the whole, Q-waveinfarctions are STEMIs and non-Q waveinfarctions are NSTEMIs. However, there isnow treatment (PCI or thrombolysis) that canprevent Q wave development in a STEMI,making the Q/non-Q differentiation redundant.

REMINDERS

STEMI

Sequence of ECG changes

1. Normal ECG.

2. Raised ST segments.

3. Appearance of Q waves.

4. Normalization of ST segments.

5. Inversion of T waves.

Site of infarction

∑ Anterior infarction: changes classically in leads V3–V4,

but often also in leads V2 and V5.

∑ Inferior infarction: changes in leads III and VF.

∑ Lateral infarction: changes in leads I, VL and V5–V6.

∑ True posterior infarction: dominant R waves in lead V1.


143

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.12

Anterior non-ST segment elevation myocardial infarctionNote


∑ Normal axis

∑ Normal QRS complexes and ST segments

∑ T wave inversion in leads I, VL and V3–V6

∑ This pattern must be differentiated from that of left ventricular hypertrophy, where it would be most

unusual to see T wave inversion in leads V3–V4

144



INTERMITTENT CHEST PAIN

Patients with angina may have a normal ECGwhen they are pain-free, although frequentlythe ECG shows evidence of a previous infarction.Patients whose chest pain is due to oesophagealdisease or to muscular disorders, or whose painis ‘nonspecific’, will also have a normal ECG.

In angina the ST segment typically becomesdepressed, but when the angina is due tocoronary vasospasm the ST segment maybecome elevated (‘Prinzmetal’s variant angina’).If a diagnosis of angina is in doubt, ECG changescan be induced by exercise. Exercise testing isless sensitive than, and is now being replacedby, stress echocardiography (and in somecardiologists’ minds by immediate coronaryangiography). However, exercise testing stillhas an important role in demonstrating apatient’s tolerance to exercise, and in findingout just what limits him or her. Exercise testinghas great advantages over coronary angiography:it is noninvasive, and the detection of coronarylesions during angiography does not necessarilymean that they are responsible for the patient’ssymptoms.

Exercise testing can be performed on atreadmill or an exercise bicycle, the formerbeing more commonly used in the UK. Afterrecording the ECG at rest, exercise isprogressively increased in stages of 3 min. Themost commonly used protocol is that devised byBruce (Table 6.1). The two low-level stages (the‘modified Bruce protocol’), both at 2.7 kph but

with a 0% or 5% gradient, can be used when apatient’s exercise tolerance is markedly limited.

The heart rate, blood pressure and 12-leadECG are recorded at the end of each stage.Exercise is continued until the patient asks tostop, but the test is ended early if the systolicblood pressure falls by more than 20 mmHg orthe heart rate falls by more than 10/min. Thetest should also be ended if the patient developschest pain and the ST segment in any lead isdepressed by 2 mm, or if it is depressed by morethan 3 mm without chest pain. The onset of anyconduction disturbance or arrhythmia is also anindication for immediate discontinuation.

A diagnosis of cardiac ischaemia canconfidently be made if there is horizontal STsegment depression of at least 2 mm. If the STsegments are depressed but upward-sloping,there is probably no ischaemia. Figures 6.13 and6.14 show the ECG of a patient at rest and afterexercise causing angina.

Table 6.1 Bruce protocol

Stage Speed Speed Gradient

(kph) (mph) (degrees)

01 2.7 1.7 0

02 2.7 1.7 5

1 2.7 1.7 10

2 4.0 2.5 12

3 5.4 3.4 14

4 6.7 4.2 16

5 8.0 5.0 18

ECGIP

For more on

exercise testing,

see pp. 270–284

6The ECG in patients with intermittent chest pain

145

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.13

At restNote


∑ Normal axis


146


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 6.14

After 5 min of exercise (same patient as in Fig. 6.13)Note


∑ Left axis deviation

∑ Horizontal ST segment depression in the inferior and anterior leads, with a maximum of 4 mm in lead V5

6The ECG in patients with breathlessness

147


BREATHLESSNESS

Some causes of breathlessness are summarizedin Box 6.3.

BREATHLESSNESS DUE TO HEART DISEASE

Remember that, although no particular ECGpattern corresponds to heart failure, thiscondition is unlikely with a completely normalECG – other explanations for breathlessnessshould be considered. ECG evidence of cardiacenlargement may point to the cause ofbreathlessness. For example, ECG evidence of left ventricular hypertrophy may be due tohypertension or to mitral or aortic valve disease.

When the ECG of a breathless patient showsan arrhythmia or a conduction abnormality, orevidence of ischaemia or of atrial or ventricularhypertrophy, then the breathlessness may bedue to heart failure.

∑ Lack of physical fitness

∑ Obesity

∑ Heart failure

∑ Lung disease

∑ Anaemia

∑ Neuromuscular disorders

∑ Chest wall pain

Box 6.3 Causes of breathlessness

REMINDERS

CARDIAC HYPERTROPHY

Right atrial hypertrophy

∑ Peaked P waves.

Right ventricular hypertrophy

∑ Tall R waves in lead V1.

∑ T wave inversion in leads V1 and V2, andsometimes in V3 and even V4.

∑ Deep S waves in lead V6.

∑ Right axis deviation.

∑ Sometimes, right bundle branch block.

Left atrial hypertrophy

∑ Bifid P waves.

Left ventricular hypertrophy

∑ R waves in lead V5 or V6 greater than 25 mm.

∑ R waves in lead V5 or V6 plus S waves in leadV1 or V2 greater than 35 mm.

∑ Inverted T waves in leads I, VL, V5–V6 and,sometimes, V4.

148


BREATHLESSNESS DUE TO LUNG DISEASE

Pulmonary embolism

Pulmonary embolism often presents as acombination of chest pain and breathlessness.Although the chest pain is characteristicallyone-sided and pleuritic, a major embolusaffecting the main pulmonary arteries may causepain resembling that of myocardial infarction.Patients with pulmonary hypertension usuallycomplain of breathlessness but not pain.

With pulmonary embolism the most commonECG finding is sinus tachycardia with no otherabnormality (Fig. 6.15), so the ECG is not avery useful diagnostic tool. However, theappearance of right bundle branch block, or the changes associated with right ventricularhypertrophy (right axis deviation, a dominantR wave in lead V1, and T wave inversion inleads V1–V3) would strongly support thediagnosis. If the patient develops permanentpulmonary hypertension, the full ECG pictureof right ventricular hypertrophy will persist.

The commonly quoted ‘S1Q3T3’ pattern (i.e.right axis deviation with a prominent S wave in

lead I and a Q wave and an inverted T wave inlead III) is seen in Figure 6.15, and is commonlyquoted as an indicator of pulmonary embolism.In practice, it is not a very reliable indicatorunless it is seen to appear in repeated recordings.

REMINDERS

PULMONARY EMBOLISM

Possible ECG patterns include:

∑ Normal ECG with sinus tachycardia

∑ Peaked P waves


∑ Right bundle branch block

∑ Dominant R waves in lead V1 (i.e. R wavebigger than S wave)

∑ Inverted T waves in leads V1–V3

∑ Deep S waves in lead V6

∑ Right axis deviation (S waves in lead I), plusQ waves and inverted T waves in lead III.

ECGIP

For more on

pulmonary

embolism, see

pp. 247–250

6The ECG in patients with breathlessness

149

V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 6.15

Pulmonary embolismNote


∑ Right axis deviation (QRS complexes predominantly downward in lead I)

∑ Peaked P waves in lead II, suggesting right atrial hypertrophy

∑ Persistent S wave in lead V6

∑ T waves inverted in leads V1, V5, II, III and VF

∑ Right bundle branch block pattern

150


VRI

VLII

VFIII

V1 V4

V2 V5

V3 V6

Fig. 6.16

Chronic lung diseaseNote



∑ Peaked P waves, best seen in leads V1–V2

∑ Partial right bundle branch block

∑ Deep S waves in lead V6, with no chest lead showing a pattern suggestive of left ventricular hypertrophy

Chronic lung disease

Chronic obstructive pulmonary disease,pulmonary fibrosis and other intrinsic lungdiseases do not usually cause the ECG changesassociated with severe pulmonary hypertension,

but there may be right axis deviation and, more often, clockwise rotation of the heart(Fig. 6.16). This is because the heart is rotated,with the right ventricle occupying more of theprecordium than usual.

The ECG in patients withpalpitations or syncope

The ECG when the patient has no

symptoms 151

The ECG when the patient has symptoms 164

Pacemakers 169

Cardiac arrest 173

‘Palpitations’ means different things todifferent people, but essentially it means anawareness of the heartbeat. ‘Syncope’ meanssudden loss of consciousness. The only way ofbeing certain that a cardiac problem is thecause of either phenomenon is to record anECG when the patient is having a typicalattack, but this is seldom possible. Nevertheless,the ECG can be helpful, even when the patientis well.

THE ECG WHEN THE PATIENT HAS

NO SYMPTOMS

If a patient is well at the time of recording, fourpossible ECG patterns can point to a diagnosis:

∑ Normal∑ Patterns suggesting cardiac disease∑ Patterns suggesting paroxysmal tachycardia∑ Patterns suggesting syncope due to

bradycardia.

NORMAL ECGs

Symptoms may not be due to heart disease – thepatient may have epilepsy or some othercondition. However, a normal ECG does not ruleout a paroxysmal arrhythmia, and the patient’sdescription of his or her symptoms may be

151

7

152

The ECG in patients with palpitations or syncope

crucial. For example, if the patient’s attacks areassociated with exercise (think of anaemia) oranxiety, and the palpitations build up and slowdown, sinus tachycardia is likely to be the causeof the symptoms. In paroxysmal tachycardia,the attack begins suddenly, often for no obviousreason, and may stop suddenly. Ambulatoryrecording over 24 h, using, for example, theHolter technique, may be necessary to obtain arecord of an attack (Fig. 7.1).

PATTERNS SUGGESTING CARDIACDISEASE

Marked T wave inversion may suggest either leftventricular hypertrophy or left bundle branchblock, which may be due to aortic stenosis; orright ventricular hypertrophy, which may be

due to pulmonary hypertension. In a youngperson, who is unlikely to have coronary disease,this pattern pattern suggests hypertrophiccardiomyopathy (Fig. 7.2), which is associatedwith arrhythmias, syncope and sudden death.

PATTERNS SUGGESTING PAROXYSMALTACHYCARDIA

Pre-excitation syndromes

A PR interval that is short (less than 120 ms),with a wide and abnormal QRS complex,indicates the Wolff–Parkinson–White (WPW)syndrome. A short PR interval with a normalQRS complex suggests the Lown–Ganong–Levine(LGL) syndrome. In both cases an abnormalpathway bypasses the atrioventricular (AV) node,causing the short PR interval.

II

Fig. 7.1

Ambulatory recording: broad complex tachycardiaNote

∑ Ambulatory records provide only one or two leads, showing rhythm strips


∑ One ventricular extrasystole

∑ A nine-beat run of broad complex tachycardia, probably ventricular in origin

7The ECG when the patient has no symptoms

153

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.2

Hypertrophic cardiomyopathyNote


∑ Normal axis

∑ Left ventricular hypertrophy on voltage criteria (S wave in lead V1 = 28 mm, R wave in lead V5 = 30 mm)

∑ Deep T wave inversion in leads I, II, VL and V3–V6, maximal in lead V4

∑ This ECG could be due to left ventricular hypertrophy rather than hypertrophic cardiomyopathy, but the

T wave inversion is dramatic and is maximal in lead V4 rather than in V6. Anterolateral ischaemia is also

unlikely, because of the marked nature of the T wave inversion

154


In the WPW syndrome, the abnormalpathway connects the atrium and the ventricle,and the QRS complex is wide, with a slurredupstroke. In the WPW syndrome type A, thepathway is left-sided, connecting the leftatrium and left ventricle, and causes adominant R wave in lead V1 (Fig. 7.3; for

another example see Fig. 3.28). This may beconfused with right ventricular hypertrophy.Less commonly, the abnormal pathway can beright-sided, connecting the right atrium andright ventricle, and this is called the WPWsyndrome type B (Fig. 7.4). Here, lead V1 hasno dominant R wave but has a deep S wave,

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.3

The Wolff–Parkinson–White syndrome type ANote


∑ Normal axis

∑ Short PR interval (100 ms)

∑ QRS complexes slightly prolonged, at 130 ms; upstroke is slurred

(best seen in leads V4–V5)



155

VRI

VLII

VFIII

V1 V4

V2 V5

V3 V6

Fig. 7.4

The Wolff–Parkinson–White syndrome type BNote

∑ Sinus rhythm, rate 55/min – P waves best seen in lead V1

∑ The first complex is probably a ventricular extrasystole

∑ Short PR interval


∑ Broad QRS complexes (160 ms) with a slurred upstroke (delta wave), seen best in leads V2–V4

∑ Inverted T waves in leads I, II and VL, and biphasic T waves in leads V5–V6

∑ The small second and third complexes in lead II appear to be due to a technical error

∑ This record must be distinguished from sinus rhythm with left bundle branch block, and from the

Wolff–Parkinson–White syndrome type A

and there is anterior T wave inversion, whichmay lead to a mistaken diagnosis of anteriorischaemia. The wide QRS complex seen in bothtypes of the WPW syndrome may also lead to amistaken diagnosis of bundle branch block,although the characteristic ‘M’ pattern of the

QRS complexes in left bundle branch block isnot seen in the WPW syndrome.

In the LGL syndrome the abnormal pathwayconnects the atria to the His bundle, so there isa short PR interval but a normal QRS complex(Fig. 7.5).

156


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.5

The Lown–Ganong–Levine syndromeNote


∑ Normal axis

∑ Short PR interval, 100 ms

∑ Normal QRS complexes and T waves

∑ In the LGL syndrome the accessory pathway connects the atria to the His bundle rather than to the

right or left ventricle, so the QRS complex is normal


157

Congenital

∑ Jervell–Lange–Nielson syndrome

∑ Romano–Ward syndrome

∑ Several other genetic abnormalities also identified

Antiarrhythmic drugs

∑ Procainamide

∑ Disopyramide

∑ Amiodarone

∑ Sotalol

Box 7.1 Causes of prolonged QT interval

Other drugs

∑ Tricyclic antidepressants

∑ Erythromycin

Plasma electrolyte abnormalities

∑ Low potassium

∑ Low magnesium

∑ Low calcium

Long QT interval

The QT interval varies with the heart rate (andalso with gender and the time of day). Thecorrected interval (QTc) can be calculatedusing Bazett’s formula:

QTc = QT

÷(R–R interval)

A QTc interval longer than 450 ms is likelyto be abnormal. QT interval prolongation canbe congenital, but is most often due to drugs,particularly to antiarrhythmic drugs (Box 7.1and Fig. 7.6).

Whatever its cause, a corrected QT interval of500 ms or longer can predispose to paroxysmalventricular tachycardia of a particular type called‘torsade de pointes’, which can cause eithersymptoms typical of paroxysmal tachycardia orsudden death. Figure 7.7 shows a continuousECG from a patient who was being treatedwith an antiarrhythmic drug and who developedventricular fibrillation while being monitored.A few seconds before the cardiac arrest, hedeveloped a transient broad complex tachycardiain which the QRS complexes were initiallyupright but then changed, to becomedownward-pointing. This is typical of ‘torsadede pointes’ ventricular tachycardia.

158


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.6

Prolonged QT intervalNote


∑ Normal axis

∑ P wave difficult to see in some leads, but most obvious in leads I and VL


∑ T wave inversion in leads I, VL and V1–V6

∑ QT interval 480 ms, QTc interval 520 ms

∑ In this patient the prolonged QT interval was due to amiodarone


159

Fig. 7.7

Torsade de pointes ventricular tachycardia and ventricular fibrillationNote

∑ The three rhythm strips are a continuous record

∑ The underlying rhythm is sinus, rate about 100/min

∑ In the top strip there are one supraventricular extrasystole (arrowed) and three ventricular extrasystoles

∑ In the second strip there is a run of broad complex tachycardia, with the first four QRS complexes pointing

upwards and the reminder pointing downwards – this is typical of torsade de pointes tachycardia

∑ In the bottom strip there is a single ventricular extrasystole and then ventricular fibrillation develops

∑ In this record a prolonged QT interval is not obvious – the QT interval is best measured on a 12-lead ECG

160


Sinoatrial disease

Sinoatrial disease, known as the ‘sick sinus’syndrome, typically causes an inappropriate sinusbradycardia but is often asymptomatic (Fig. 7.8).It can also be associated with a variety of

conduction problems, escape rhythms orparoxysmal tachycardia (Box 7.2). Patients maytherefore complain of either dizziness, syncopeor symptoms suggesting paroxysmal tachycardia.

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.8

Sick sinus syndromeNote

∑ Look at the rhythm strip first

∑ The first three beats are due to AV nodal escape, with a rate of 35/min

∑ P waves can be seen immediately before or immediately after the QRS complex

∑ The next three beats are in sinus rhythm, rate 38/min

∑ The QRS complexes and T waves are normal

∑ A combination of sinus bradycardia and AV nodal escape is typical of the sick sinus syndrome

PATTERNS SUGGESTING SYNCOPE DUETO BRADYCARDIA

In apparently healthy subjects who complain of attacks of dizziness, the resting ECG whenasymptomatic may show axis deviation, sicksinus syndrome or any variety of heart block.First degree block, second degree block of the Wenckebach (Mobitz type 1) variety, andbundle branch block do not in themselvesindicate treatment, and neither do combinationsof these blocks, such as first degree block andbundle branch block (Fig. 7.9), or bifascicularblock (left anterior hemiblock and right bundlebranch block, Fig. 7.10). However, suchcombinations may also be associated with higherdegrees of block, and ambulatory recording may

be considered to see if second or third degreeblock is occurring intermittently.

In a patient with second degree block(Mobitz type 2, 2:1 block or 3:1 block) orcomplete (third degree) block, it is likely thatany dizziness or syncope is due to a low heartrate, and pacing is indicated without the needfor ambulatory recording first.

It is important to consider the possibleunderlying causes of heart block, and these aresummarized in Box 7.3.


161

∑ Inappropriate sinus bradycardia

∑ Sudden changes in the sinus rate

∑ Sinus pauses

∑ Atrial standstill

∑ Atrioventricular junctional escape rhythms

∑ Junctional tachycardia alternating with

junctional escape

Box 7.2 Cardiac rhythms associated with sick

sinus syndromeFirst and second degree block

∑ Increased vagal tone

∑ Athletes

∑ Acute myocarditis

∑ Ischaemic heart disease

∑ Hypokalaemia

∑ Digoxin

∑ Beta-blockers

Complete block

∑ Idiopathic (fibrosis of conduction tissue)

∑ Congenital

∑ Ischaemic heart disease

∑ Aortic stenosis

∑ Surgery and trauma

Box 7.3 Causes of heart block

162


V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.9

First degree block and left bundle branch blockNote


∑ Normal axis

∑ Prolonged PR interval, 224 ms

∑ Wide QRS complexes

∑ ‘M’ pattern in leads I, II, V5 and V6

∑ Inverted T waves in leads I, VL and V6


163

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.10

Bifascicular blockNote


∑ Left axis deviation (S wave greater than R wave in leads II and III)

∑ Right bundle branch block – wide QRS complexes (135 ms); RSR1 pattern in lead V1; and a wide slurred

S wave in lead V6

THE ECG WHEN THE PATIENT HAS

SYMPTOMS

PAROXYSMAL TACHYCARDIA

It is not possible to tell from a patient’s symptomswhether extrasystoles or a paroxysmal tachycardiaare supraventricular or ventricular in origin –although paroxysmal ventricular tachycardia isperhaps more likely to cause dizziness orsyncope than paroxysmal supraventriculartachycardia.

In a paroxysmal tachycardia, the heart rate isusually greater than 160/min – compared withsinus tachycardia, in which it is seldom greaterthan 140/min. The QRS complexes in paroxysmaltachycardia can be narrow (i.e. less than120 ms) or broad.

Narrow complex tachycardias may indicate:

∑ Sinus tachycardia∑ Atrial tachycardia∑ Junctional (AV nodal re-entry) tachycardia∑ Atrial flutter∑ Atrial fibrillation∑ The WPW syndrome.

The ECG characteristics of the supraventricularrhythms are summarized in the Reminders onpage 165.

The simplest way to identify the cause ofnarrow complex tachycardia is to apply carotidsinus pressure while recording an ECG. Thiswill cause sinus tachycardia to slow; atrial andjunctional tachycardias and tachycardias due topre-excitation may be abolished; in atrial flutterthe atrioventricular block will increase; and

atrial fibrillation will not usually be affected(see p. 72).

Broad complex tachycardias indicate:

∑ Ventricular tachycardia ∑ Supraventricular tachycardia of any type

(other than sinus rhythm) with bundlebranch block

∑ The WPW syndrome.

164


REMINDERS

THE VENTRICULAR RHYTHMS

∑ In general, ventricular rhythms have wide(greater than 120 ms) QRS complexes; achange of axis compared to sinus rhythm;and abnormal T waves.

∑ Ventricular extrasystoles:

– early QRS complex

– no P wave

– QRS complex wide (greater than 120 ms)

– abnormally shaped QRS complex

– abnormally shaped T wave

– next P wave is on time.

∑ Accelerated idioventricular rhythm:

– no P wave

– QRS rate less than 120/min.

∑ Ventricular tachycardia:

– no P waves

– QRS rate greater than 160/min.

∑ Ventricular fibrillation:

– look at the patient, not at the ECG.

7The ECG when the patient has symptoms

165

REMINDERS

THE SUPRAVENTRICULAR RHYTHMS

∑ Atrial flutter:

– P wave rate 300/min

– sawtoothed pattern

– 2:1, 3:1 or 4:1 block

– block increased by carotid sinus pressure.

∑ Atrial fibrillation:

– the most irregular rhythm of all

– QRS complex rate characteristically over160/min without treatment, but can beslower

– no P waves identifiable, but there is avarying, completely irregular baseline.

∑ AV nodal re-entry (junctional) tachycardia:

– commonly, but inappropriately, called‘SVT’ (supraventricular tachycardia)

– no P waves

– rate usually 150–180/min

– carotid sinus pressure may causereversion to sinus rhythm.

∑ Escape rhythms:

– bradycardias, otherwise characteristics asabove, except that atrial fibrillation doesnot occur as an escape rhythm.

∑ In general, supraventricular rhythms have

narrow (less than 120 ms) QRS complexes,the exceptions being bundle branch blockand the WPW syndrome, in which wide

QRS complexes are seen.

∑ Sinus rhythm:

– one P wave per QRS complex

– P–P interval varies with respiration (sinusarrhythmia).

∑ Supraventricular extrasystoles:

– early QRS complex

– no P wave, or abnormally shaped (atrial) P wave

– narrow and normal QRS complex

– normal T wave

– next P wave is ‘reset’.

∑ Atrial tachycardia:

– QRS complex rate greater than 150/min

– abnormal P waves, usually with short PRintervals

– usually one P wave per QRS complex, butsometimes P wave rate 200–240/min,with 2:1 block.

It can be very difficult to differentiatebetween the broad complexes of asupraventricular tachycardia with bundle

The ECG characteristics of the broadcomplex tachycardias are summarized in theReminders on page 164.

branch block and ventricular tachycardia, butthe following Reminders should help.

Figure 7.11 shows an ECG with all the usualfeatures of ventricular tachycardia – left axis

deviation, QRS complexes with duration180 ms, and all the complexes in the chest leadspointing upwards.

INTERMITTENT BRADYCARDIA

Intermittent bradycardia due to any cardiacrhythm can cause dizziness and syncope if theheart rate is low enough. Athletes can beperfectly healthy with a sinus rate of 40/min,but an elderly person may become dizzy if theheart rate drops below 60/min for any reason.

A low rate can be due to second or thirddegree heart block (see pp. 37–42) or to ‘pauses’,when the sinoatrial node fails to depolarize.This is seen in the sick sinus syndrome. Figure7.12 shows an ambulatory record from a patientwith sick sinus syndrome, who complained ofattacks of dizziness which were due to sinuspauses of 3.3 s.

There is no effective medical treatment forsymptomatic bradycardia, and permanent pacingmay be necessary.

In the context of acute myocardial infarction,particularly inferior ST segment elevationmyocardial infarction (STEMI), complete heartblock is not uncommon. It is usually temporary,and does not need pacing unless there ishaemodynamic impairment due to a slow heartrate. When complete block complicates ananterior STEMI, a large amount of myocardiumhas usually been damaged, and temporarypacing may be needed.

166


REMINDERS

BROAD COMPLEX TACHYCARDIAS

∑ When seen in the context of acutemyocardial infarction, a broad complextachycardia is likely to be ventricular in origin.

∑ Comparison with a record made duringsinus rhythm (if available) will show ifbundle branch block is normally present.

∑ Try to identify P waves.

∑ Left axis deviation with right bundle branchblock is usually indicates a ventricularproblem.

∑ Very wide (greater than 160 ms) QRScomplexes usually indicate ventriculartachycardia.

∑ Concordance – ventricular tachycardia is likely if the QRS complexes all pointpredominantly upwards or downwards in the chest leads.

∑ An irregular broad complex rhythm is likelyto be atrial fibrillation with bundle branchblock, or atrial fibrillation in the WPWsyndrome (a dangerous combination).

7The ECG when the patient has symptoms

167

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.11

Ventricular tachycardiaNote

∑ Regular broad complex tachycardia, rate 200/min

∑ No P waves visible


∑ QRS complex duration 180 ms (if >160 ms, the rhythm is more likely to be ventricular in origin than

to be supraventricular with bundle branch block)

∑ QRS complexes all point the same way (upwards) in the chest leads (again, makes a ventricular

origin likely)

168


Fig. 7.12

Ambulatory record, sick sinus syndromeNote

∑ The first two beats demonstrate sinus rhythm, rate 38/min

∑ The third beat is an atrial extrasystole, shown by an abnormal P wave

∑ There is then a prolonged pause lasting 3.5 s, followed by another sinus beat

PACEMAKERS

Pacemakers produce a small electrical dischargethat either replaces the function of the sinoatrialnode or bypasses a blocked His bundle. Thesophisticated design of pacemakers enablesthem to mimic many of the functions of thenormal heart.

Pacemaker function can be assessed from theresting ECG. Most modern pacemakers sensethe intrinsic activation of the atria and/or theventricles, and may pace both. The operatingmode of a pacemaker can be described in threeor four letters:

1. The first letter describes the chamber(s)paced (A for right atrium, V for rightventricle or D for dual, i.e. both chambers).

2. The second letter describes the chamberssensed (A, V or D).

3. The third letter describes the response to asensed event (A, V or D for pacing; I forpacemaker inhibition).

4. The fourth letter (R) is used when the ratemodulation is programmable.

Thus, ‘VVI’ means that the pacemaker paces and senses the right ventricle. When nospontaneous activity is sensed, the pacemakerstimulates the right ventricle; and whenspontaneous activity is sensed, the pacemaker isinhibited. The ECG looks like that in Figure 7.13.

‘AAI’ means that the pacemaker has a singlelead in the atrium, to both sense and pace it(Fig. 7.14). If the pacemaker does not sensespontaneous atrial depolarization, it stimulatesthe atrium; and when there is spontaneousdepolarization, the pacemaker is inhibited.

‘DDD’ means that there are pacemaker leadsin both the right atrium and the right ventricle,and both chambers are sensed and paced. If noatrial activity is sensed within a predeterminedperiod, the atrial pacing lead will pace. Amaximum PR interval is also predetermined,and if no ventricular beat is sensed, the ventriclewill be paced. Figure 7.13 could be the result of simple VVI pacing, or could be the result ofatrial sensing and ventricular pacing, theventricular rate ‘following’ the atrial rate. Achest X-ray would show whether there wereone or two pacing leads. Figure 7.15 showsboth atrial and ventricular pacing.

7Pacemakers

169

170


V1 V4VRI

V2 V5VLII

V3 V6VFIII

VI

Fig. 7.13

Ventricular pacingNote

∑ Ventricular paced rhythm: there is a sharp pacemaker spike before each QRS complex

∑ The QRS complexes are wide and abnormal

∑ Sinus rate, 75/min

∑ Prolonged PR interval, 280 ms

∑ Each paced beat follows a P wave

∑ This could be VVI pacing, but the pacemaker is probably tracking the atrial rate by means of a sensing

catheter in the right atrium (DDD pacing)

7Pacemakers

171

V1 V4VRI

V2 V5VLII

II

V3 V6VFIII

Fig. 7.14

Atrial pacingNote

∑ Atrial paced rhythm, shown by a sharp pacing spike immediately before each P wave


∑ The QRS complexes are narrow but there is a lack of R wave development in the anterior

leads, suggesting an old anterior infarction

∑ T waves inverted in leads II, VL and V4–V6, consistent with ischaemia

∑ In atrial pacing the QRS complexes and T waves can be interpreted, whereas in ventricular

pacing they are bound to be abnormal

172


V1 V4VRI

V2 V5VLII

V3 V6VFIII

Fig. 7.15

Dual chamber pacingNote

∑ Two pacing spikes can be seen, most clearly in leads V1–V3

∑ The first spike causes atrial activity, though no clear P wave can be seen

∑ The second spike causes ventricular activity, with a wide and abnormal QRS complex

7Cardiac arrest

173

anaphylactic shock (the combination of laryngealoedema, bronchospasm and hypotension), the doseis 0.5 mg given intramuscularly, because adrenalinegiven intravenously can cause cardiac arrhythmias.

The nonshockable rhythms are asystole andpulseless electrical activity (PEA). If it is notclear whether the rhythm is ‘fine’ VF orasystole, treat as VF until three defibrillationshave not changed the apparent rhythm. Thetreatment sequence after the first two steps is:

1. Adrenaline 1 mg i.v.2. CPR 30:2 for 2 min.3. Atropine 3 mg i.v.4. If unsuccessful, continue adrenaline 1 mg

after alternate 2-min cycles of CPR.

Particularly in cases of PEA, considerpossible reversible causes of cardiac arrest, allof which begin with H or T and are listed inBox 7.4.

CARDIAC ARREST

Cardiac arrest can be classified according towhether the rhythm is ‘shockable’ (i.e. correctableby DC cardioversion) or nonshockable. In eithercase, the first part of the treatment is a precordialthump and cardiopulmonary resuscitation at 30compressions for each two ventilations.

The shockable rhythms are ventricularfibrillation (VF) and pulseless ventriculartachycardia (VT). Action in either case, followingthe first two steps, should be:

1. Precordial thump.2. One shock at 200 J.3. Resume chest compressions at 30:2 for

2 min, then check the rhythm.4. If unsuccessful, defibrillate at 360 J.5. If unsuccessful, give adrenaline 1 mg i.v.6. Defibrillate at 360 J.7. 2 min of cardiopulmonary rescuscitation

(CPR).8. If VF or pulseless VT persists, give

amiodarone 300 mg i.v.9. Give further shocks after 2-min periods of

CPR, with adrenaline 1 mg i.v. beforealternate shocks.

10. For refractory VF, give magnesium sulfate2 g i.v. bolus (8 mmol).

Note that adrenaline is given intravenously onlyfor cardiac arrest. When adrenaline is given for

∑ Hypoxia

∑ Hypovolaemia

∑ Hyperkalaemia, hypokalaemia, hypocalcaemia,

acidosis, hypoglycaemia

∑ Hypothermia

∑ Tamponade

∑ Tension pneumothorax

∑ Toxic substances, including drug overdoses

∑ Thromboembolism, e.g. pulmonary embolism

Box 7.4 Causes of nonshockable rhythms

174

8 Now test yourself

ECGs with clinical scenarios 179

ECG descriptions and interpretations 185

You should now be able to recognize thecommon ECG patterns, and this final chaptercontains ten 12-lead records for you to interpret.But do not forget two important things: first,an ECG comes from an individual patient andmust be interpreted with the patient in mind,and second, there is little point in recordingand interpreting an ECG unless you areprepared to take some action based on yourfindings. This is a theme developed in thecompanion to this book, 150 ECG Problems.

When reporting an ECG, remember:

1. The ECG is easy.2. A report has two parts – a description and

an interpretation.

3. Look at all the leads, and describe the ECGin the same order every time:rate and rhythm– conduction– PR interval if sinus rhythm – cardiac axis– QRS complexes:∑ duration∑ height of R and S waves∑ presence of Q waves

– ST segments– T waves.

4. The range of normality, and especiallywhich leads can show an inverted T wave ina normal ECG.

Only after carefully thinking about everyaspect of the ECG pattern, and the patient’shistory, should you make a diagnosis. You mayfind the Reminders displayed below helpful.

8Reminders

175

REMINDERS

WHAT TO LOOK FOR

1. The rhythm and conduction:

∑ sinus rhythm or some early arrhythmias

∑ evidence of first, second or third degereeblock

∑ evidence of bundle branch block.

2. P wave abnormalities:

∑ peaked, tall – right atrial hypertrophy

∑ notched, broad – left atrial hypertrophy.

3. The cardiac axis:

∑ right axis deviation – QRS complexpredominantly downward in lead I

∑ left axis deviation – QRS complexpredominantly downward in leads II and III.

4. The QRS complex:

∑ width:

– if wide, ventricular origin, bundle branchblock or the WPW syndrome

∑ height:

– tall R waves in lead V1 in right ventricularhypertrophy

– tall R waves in lead V6 in left ventricularhypertrophy

∑ transition point:

– R and S waves are equal in the chestleads over the interventricular septum(normally lead V3 or V4)

– clockwise rotation (persistent S wave inlead V6) indicates chronic lung disease.

∑ Q waves:

– ? septal

– ? infarction.

5. The ST segment:

∑ raised in acute myocardial infarction andin pericarditis

∑ depressed in ischaemia and with digoxin.

6. T waves:

∑ peaked in hyperkalaemia

∑ flat, prolonged, in hypokalaemia

∑ inverted:

– normal in some leads

– ischaemia

– infarction

– left or right ventricular hypertrophy

– pulmonary embolism

– bundle branch block.

7. U waves:

∑ can be normal

∑ hypokalaemia.

176

Now test yourself

REMINDERS

CONDUCTION PROBLEMS

First degree block

∑ One P wave per QRS complex.

∑ PR interval greater than 200 ms.

Second degree block

∑ Wenckebach (Mobitz type 1): progressivePR lengthening then a nonconducted P wave,and then repetition of the cycle.

∑ Mobitz type 2: occasional nonconductedbeats.

∑ 2:1 (or 3:1) block: two (or three) P waves perQRS complex, with a normal P wave rate.

Third degree (complete) block

∑ No relationship between P waves and QRScomplexes.

∑ Usually, wide QRS complexes.

∑ Usual QRS complex rate less than 50/min.

∑ Sometimes, narrow QRS complexes, rate50–60/min.


∑ QRS complex duration greater than 120 ms.

∑ RSR1 pattern.

∑ Usually, dominant R1 wave in lead V1.

∑ Inverted T waves in lead V1, and sometimesin leads V2–V3.

∑ Deep and wide S waves in lead V6.

Left anterior hemiblock

∑ Marked left axis deviation – deep S wavesin leads II and III, usually with a slightlywide QRS complex.


∑ QRS complex duration greater than 120 ms.

∑ ‘M’ pattern in lead V6, and sometimes inleads V4–V5.

∑ No septal Q waves.

∑ Inverted T waves in leads I, VL, V5–V6 and,sometimes, V4.

Bifascicular block

∑ Left anterior hemiblock and right bundlebranch block (see above).

8Reminders

177

REMINDERS

CAUSES OF AXIS DEVIATION

Right axis deviation

∑ Normal variant – tall thin people.

∑ Right ventricular hypertrophy.

∑ Lateral myocardial infarction (peri-infarctionblock).

∑ Dextrocardia or right/left arm lead switch.

∑ The Wolff–Parkinson–White (WPW) syndrome.

∑ Left posterior fascicular block.

Left axis deviation

∑ Left anterior hemiblock.


∑ Inferior myocardial infarction (peri-infarctionblock).

∑ Ventricular tachycardia.

REMINDERS

POSSIBLE IMPLICATIONS OF ECG PATTERNS

P:QRS apparently not 1:1

If you cannot see one P wave per QRS complex,consider the following:

∑ If the P wave is actually present but not easilyvisible, look particularly at leads II and V1.

∑ If the QRS complexes are irregular, the rhythmis probably atrial fibrillation, and what seem tobe P waves actually are not.

∑ If the QRS complex rate is rapid and there areno P waves, a wide QRS complex indicatesventricular tachycardia, and a narrow QRScomplex indicates atrioventricular nodal (junctional or AV nodal) re-entry tachycardia.

∑ If the QRS complex rate is low, it is probablyan escape rhythm.

P:QRS more than 1:1

If you can see more P waves than QRScomplexes, consider the following:

∑ If the P wave rate is 300/min, the rhythm isatrial flutter.

∑ If the P wave rate is 150–200/min and thereare two P waves per QRS complex, therhythm is atrial tachycardia with block.

∑ If the P wave rate is normal (i.e. 60–100/min)and there is 2:1 conduction, the rhythm issinus with second degree block.

∑ If the PR interval appears to be different witheach beat, complete (third degree) heartblock is probably present.

continued

REMINDERS

POSSIBLE IMPLICATIONS OF ECG PATTERNS – continued

Wide QRS complexes (greater than 120 ms)

Wide QRS complexes are characteristic of:

∑ Sinus rhythm with bundle branch block

∑ Sinus rhythm with the WPW syndrome

∑ Ventricular extrasystoles

∑ Ventricular tachycardia

∑ Complete heart block.

Q waves

∑ Small (septal) Q waves are normal in leadsI, VL and V6.

∑ A Q wave in lead III but not in VF is a normalvariant.

∑ Q waves probably indicate infarction ifpresent in more than one lead, are longerthan 40 ms in duration and are deeperthan 2 mm.

∑ Q waves in lead III but not in VF, plus rightaxis deviation, may indicate pulmonaryembolism.

∑ The leads showing Q waves indicate the siteof an infarction.

ST segment depression

∑ Digoxin: ST segment slopes downwards.

∑ Ischaemia: flat ST segment depression.

T wave inversion

∑ Normal in leads III, VR and V1; and in V2–V3

in black people.

∑ Ventricular rhythms.

∑ Bundle branch block.

∑ Myocardial infarction.

∑ Right or left ventricular hypertrophy.


178

Now test yourself

8ECGs with clinical scenarios

ECGs WITH CLINICAL SCENARIOS

The following ECGs (1–10) are in no particularsequence, and similar ECGs have been described

earlier in this book. With each there is a shortclinical scenario, and their descriptions andinterpretations commence on p. 185.

179

I VR V1 V4

II VL V2 V5

III VF V3 V6

II

ECG 1

ECG from a 20-year-old female student with nonspecific chest pain; no abnormalities on examination

180

Now test yourself

V1 V4VRI

V2 V5VLII

V3

V6VFIII

ECG 2

ECG from a student with an ejection systolic murmur and a widely split second heart sound

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 3

ECG from an 80-year-old woman who complained of dizziness. Otherwise she was well


181

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 5

ECG from a 60-year-old man who had had severe chest pain 2 days earlier

I VR V1 V4

II VL V2 V5

III VF V3 V6

ECG 4

ECG from a man in a CCU with a myocardial infarction, who suddenly became breathless with more chest pain

182

Now test yourself

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 6

ECG from a 60-year-old man who noticed dizziness and chest discomfort on climbing hills

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 7

ECG from a small 70-year-old woman with heart failure, whose main complaints were nausea and lethargy


183

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 8

ECG from a 30-year-old man with hypertension. The pulses in his legs were difficult to feel

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 9

ECG from a 25-year-old man with palpitations, breathlessness and dizziness

184

Now test yourself

V1 V4VRI

V2 V5VLII

V3 V6VFIII

ECG 10

ECG from a 50-year-old man with severe chest pain for 2 h. There were no abnormal signs

8ECG descriptions and interpretations

185

ECG DESCRIPTIONS AND

INTERPRETATIONS

ECG 1

This ECG shows:

∑ Sinus rhythm; the rhythm strip (lead II)shows sinus arrhythmia

∑ The heart rate change (most obvious in leadsVF and V3) is due to sinus arrhythmia

∑ Normal PR interval, 120 ms∑ Normal axis∑ QRS complex duration 80 ms, normal height∑ ST segment isoelectric in all leads∑ T wave inversion in lead VR, but no other lead.

Interpretation of the ECG

This is a perfectly normal record in all respects.The sinus arrhythmia is clearly shown in thesection of the rhythm strip below: the change inthe R–R interval is progressive from beat tobeat. The configuration of the P wave does notchange, so there is sinus rhythm throughout.

If you did not get this right, look at p. 32.

Clinical management

The description of the pain does not sound inthe least cardiac, and a young woman is veryunlikely to have coronary disease anyway. Ifyou find yourself making a diagnosis on thebasis of an ECG that seems clinically unlikely,think about the ECG a little further. This painsounds muscular, and she only needs reassurance.

ECG 2

This ECG shows:

∑ Sinus rhythm∑ Normal PR interval∑ Normal axis∑ Wide QRS complex duration, at 160 ms∑ RSR1 pattern in lead V1

∑ Wide and notched S wave in lead V6

∑ ST segment isoelectric∑ T wave inversion in lead VR (normal), and

in leads V1–V3.

Rhythm strip (ECG 1)

186

Now test yourself


There is no problem with conduction betweenthe atria and the ventricles because the PRinterval is normal and constant. The prolongedQRS complex duration shows that there isconduction delay within the ventricles. TheRSR1 pattern in lead V1 and the deep and wideS wave in lead V6 (see the extracts from thetraces, below) are characteristic of right bundlebranch block (RBBB).

Any problems? If so, look at pp. 44–45.

Clinical management

The story raises the possibility that this youngwoman has a congenital heart problem. Fixedwide splitting of the second heart sound is theclinical manifestation of RBBB, with whichpulmonary valve closure is delayed. RBBB ischaracteristic of an atrial septal defect, and an

echocardiogram is essential to confirm thediagnosis and to help decide if, how and whenit should be closed.

ECG 3

This ECG shows:

∑ Sinus rhythm∑ Alternate conducted and nonconducted beats∑ Normal PR interval in the conducted beats∑ Left axis deviation (deep S waves in leads II

and III)∑ Wide QRS complex (duration 160 ms)∑ RSR1 pattern in lead V1

∑ Note: the sharp spikes are due to leadchanges, not to a pacemeaker.


The alternating conducted and nonconducted Pwaves indicate second degree heart block, andthis explains the slow heart rate. The left axisdeviation shows that conduction down theanterior fascicle of the left bundle branch isblocked, and the RSR1 pattern in lead V1indicates RBBB (see the extracts from thetraces, opposite page).

This was explained in Chapter 2.

Clinical management

This patient clearly has severe disease of herconduction system. Both bundle branches areaffected, and the second degree block probably

V1

V6

ECGIP

For more on

congenital heart

disease, see

pp. 320–326

RSR1 pattern and S wave (ECG 2)


187

results from disease in the His bundle. Theattacks of dizziness may be due to furtherslowing of the heart rate with the same rhythm,or may be due to intermittent complete heart

block (Stokes–Adams attacks). This could beinvestigated with a 24-h ambulatory ECGrecording, but this is not really necessary as she needs an immediate permanent pacemaker.

I

II

III

P P

VL

V1

ECGIP

For more on

pacemakers,

see pp. 187–206

Left axis deviation, RSR1 pattern and P waves (ECG 3)

188

Now test yourself

ECG 4

This ECG shows:

∑ Broad complex tachycardia at 160/min∑ No P waves visible∑ Left axis deviation∑ QRS complex duration 200 ms∑ QRS complexes all point downwards in

the chest leads∑ Artefacts in leads I and V1–V2.


The QRS complexes are broad, so this is eitherventricular tachycardia or supraventriculartachycardia with bundle branch block. Thereare no P waves, so it is not sinus rhythm or anatrial rhythm. The QRS complexes are regular,so it is not atrial fibrillation, but an AV nodalrhythm with bundle branch block is a possibility.However, the left axis deviation, and the‘concordance’ of the QRS complexes (all pointingdownwards), makes this ventricular tachycardia(see the extracts from the traces, below).

For the diagnosis of tachycardias, see p. 75.

Clinical management

In the context of a myocardial infarction, broadcomplex tachycardia is almost always ventricularin origin, and there is no need to get toopuzzled by the ECG. This patient has developedpulmonary oedema, so needs urgent treatment.While preparations are made for DCcardioversion, he could be given intravenouslidocaine and furosemide, but you should notrely on a satisfactory response to drug therapy.

ECG 5

This ECG shows:

∑ Sinus rhythm∑ Normal PR interval∑ Normal axis∑ QRS complex has Q waves in leads II, III

and VF∑ ST segment isoelectric∑ T waves inverted in leads II, III and VF.

II III

ECGIP

For more on

differentiation

of broad

complex

tachycardias,

see p. 126

Left axis deviation and QRS complexes (ECG 4)


189


The Q waves in leads III and VF, together withthe inverted T waves in those leads (see theextract from the trace, below), indicate aninferior myocardial infarction. Since the STsegment is virtually isoelectric (i.e. at thebaseline, and not elevated) the infarction is‘old’. The ECG can show this pattern at anytime after the 24 h following the infarction, sotiming the event is not possible from the ECG.

Get this one wrong? Read pp. 91–96.

Clinical management

The clinical story suggests that the infarctionoccurred 48 h previously. This patient haspresented too late for immediate treatment ofthe infarction by thrombolysis or urgentangioplasty, and he does not need pain relief orany treatment for complications. The aim ofmanagement is therefore to prevent a furtherinfarction, and he will need long-term aspirin, a

beta-blocker, an ACE (angiotensin-convertingenzyme) inhibitor and a statin. He will also needan exercise test, and a decision will need to bemade about the need for coronary angiography.

ECG 6

This ECG shows:

∑ Sinus rhythm∑ Normal PR interval∑ Normal axis∑ Wide QRS complexes, duration 200 ms∑ ‘M’ pattern in leads I, VL and V5–V6

∑ Deep S waves in leads V2–V4

∑ Biphasic or inverted T waves in leads I, VLand V5–V6


The rhythm and PR interval are normal but the wide QRS complexes show that there is aconduction delay within the ventricles. The ‘M’

III VF

ECGIP

For more on

myocardial

infarction,

see p. 212

Q waves and inverted T waves (ECG 5)

190

Now test yourself

pattern, best seen in the lateral leads (see theextract from lead V6, above) shows that this isleft bundle branch block (LBBB). In LBBB the Twaves are usually inverted in the lateral leads,and have no further significance. In the presenceof LBBB the ECG cannot be interpreted anyfurther, so it is not possible to comment on thepresence or absence of ischaemia.

If you need to check, look at pp. 43 and 45.

Clinical management

The story sounds like angina, but when angina iscombined with dizziness always think of aorticstenosis, which can also cause angina even withnormal coronary arteries. LBBB is common inaortic stenosis. A patient with aortic stenosis whois dizzy on exertion has a high risk of suddendeath, and this patient needs urgent investigationwith a view to early aortic valve replacement.

ECG 7

The ECG shows:

∑ Atrial fibrillation∑ Normal axis∑ Normal QRS complexes∑ Downward-sloping ST segments, best seen

in leads V4–V6

∑ U waves, best seen in lead V2


The completely irregular rhythm with narrowQRS complexes must be due to atrial fibrillation,even though the usual baseline irregularity isnot very obvious. The downward-sloping STsegments indicate that she is taking digoxin,which explains the good control of theventricular rate (with untreated atrial fibrillationthe ventricular rate would usually be rapid);and the U waves suggest hypokalaemia (see theextracts from the traces, opposite page: in lead V5,the downward-sloping ST segment is arrowed).

If you made a mistake with this one, readp. 101.

Clinical management

If this patient who is taking digoxin feels sick,she is probably suffering from digoxin toxicity,and hypokalaemia may be the main cause ofthis. Hypokalaemia is likely to occur if a patientwith heart failure is given a loop diureticwithout either a potassium-retaining diuretic orpotassium supplements. The serum potassium

V6

ECGIP

For more on

the ECG in

patients with

dizziness,

see Ch. 2

ECGIP

For more on

electrolyte

abnormalities,

see p. 331

‘M’ pattern (ECG 6)

V2


191

level must be checked urgently, and appropriateaction taken.

Remember that we have still not made a fulldiagnosis: what is the cause of the atrialfibrillation? Most cardiac conditions can beassociated with atrial fibrillation, but in elderlypatients the important disease to remember isthyrotoxicosis, because atrial fibrillation may bethe only manifestation of this in the elderly.

ECG 8

This ECG shows:

∑ Sinus rhythm∑ Bifid P waves∑ Normal conducting intervals

∑ Normal axis∑ Tall R wave in lead V5 and deep S wave in

lead V2

∑ Small (septal) Q wave in leads I, VL and V5–V6


∑ U waves in leads V2–V4 (normal).


The bifid P waves, best seen in lead V3, indicateleft atrial hypertrophy (see the extracts fromthe trace, p. 192). The combined height of theR wave in lead V5 plus the depth of the S wavein lead V2 is 58 mm, so there are ‘voltagecriteria’ for left ventricular hypertrophy. Theinverted T waves in the lateral leads confirmsevere left ventricular hypertrophy. The Q waves

UV5

U wave and downward-sloping ST segment (ECG 7)

ECGIP

For more on

diagnosis of left

ventricular

hypertrophy,

see pp. 295–303

ECGIP

For more on

normal variants

of the ECG,

see Ch. 1

192

Now test yourself

are small and narrow, and are therefore septalin origin and do not indicate an old infarction.

If you needed help with this one, re-readpp. 90–91.

Clinical management

This patient has clinical and ECG evidence ofleft ventricular hypertrophy, but this is not afull diagnosis – what might be the cause of thehypertension? A young man with hypertensionwho has abnormal pulses in the legs almostcertainly has a coarctation of the aorta, whichneeds investigation and correction.

ECG 9

This ECG shows:

∑ Narrow QRS complexes (duration less than120 ms)

∑ Tachycardia at 200/min

∑ No visible P waves∑ Normal QRS complexes∑ ST segments with a little depression in leads

II, III and VF∑ Normal T waves except in lead III.


The QRS complexes are narrow, so this is asupraventricular tachycardia. It is regular, so itis not atrial fibrillation. No P waves are visible,so it is not sinus rhythm, atrial tachycardia oratrial flutter (see the extract from the trace,below). This has to be an AV nodal re-entry, or junctional, tachycardia (sometimes, but not logically, referred to as ‘supraventricular’tachycardia or ‘SVT’).

In case of difficulty, look at pp. 70–71.

V3

P

V3

28 mm

V5

P wave and R wave (ECG 8)

Narrow QRS complexes and no

visible P waves (ECG 9)

Clinical management

This rhythm can often be terminated by carotidsinus pressure, or by the Valsalva manoeuvre.Failing that, it will usually respond tointravenous adenosine. DC cardioversion shouldbe considered for any patient with tachycardiathat is compromising the circulation. The bestway of preventing the attacks depends on theirfrequency and severity. An electrophysiologicalstudy, with a view to possible ablation of anabnormal conducting pathway, should beconsidered.

ECG 10

This ECG shows:

∑ Sinus rhythm∑ Normal conducting intervals ∑ Normal axis∑ Small R waves in leads V1–V2

∑ Very small R wave in lead V3

∑ Small Q wave and very small R wave inlead V4

∑ Raised ST segments in leads I, VL andV2–V5.


The small R waves in leads V1–V2 could benormal, but leads V3–V4 should show larger Rwaves. The raised ST segments indicate an STsegment elevation myocardial infarction (seethe extracts from the traces, oposite). The smallQ wave in lead V4suggests that a fairly short timehas elapsed since the onset of the infarction, and

this Q wave will probably become larger overthe next few hours. Since the changes arelimited to leads I, VL and V2–V5, this is an acuteanterolateral myocardial infarction (STEMI).

You must have got this one right – the ECGis easy!

Clinical management

This man needs urgent pain relief. Pain radiatingto the back always raises the possibility of anaortic dissection, but it is quite common in acuteinfarction, and there are no physical signs – lossof pulses, asymmetric blood pressure in the arms,a murmur of aortic regurgitation or pericarditis –to support a diagnosis of aortic dissection. If indoubt an urgent echocardiogram may help, butessentially this patient needs either immediatethrombolysis or angioplasty.

The moral of this story – and of all theothers – is that an ECG is an aid to diagnosis,not a substitute for further thought.


193

ECGIP

For more on

electrophysiology

and ablation,

see pp. 155–162

ECGIP

For more on

myocardial

infarction, see

pp. 214–246

ECG150

If you find

testing yourself

helpful, try

150 ECG Problems

V3 V4

R wave and Q wave (ECG 10)

194

A

‘AAI’ pacing 169accelerated idioventricular rhythm 60, 63,

164accessory conducting bundle 79acute coronary syndrome 129–30

unstable angina 129, 130see also myocardial infarction

adrenaline 173ambulatory (ECG) record

paroxysmal tachycardia 152sick sinus syndrome 166, 168syncope due to bradycardia 161

anaphylactic shock 173angina 128, 129, 130, 131, 144

dizziness with 190ECG at rest 145exercise causing 146unstable 129, 130

anterior axillary line 22anterior fascicle of left bundle branch 49,

49block, see left anterior hemiblock

antiarrhythmic drugs, prolonged QTinterval due to 157, 157

aortic dissection 193aortic stenosis 152, 161, 190arrhythmia 56, 58–9

ECG abnormality summary 83, 84junctional (nodal) 58–9management 82–3

left see left atrial hypertrophy right see right atrial hypertrophy

atrial muscle, abnormal rhythms arising58, 59

atrial pacing 169, 171atrial rates of discharge, tachycardia 66, 67atrial rhythm, ectopic 111, 111atrial septal defect 116, 117, 186atrial tachycardia 66–7, 67, 165

2:1 block with 67, 68, 69carotid sinus pressure in 82

atrioventricular (AV) block 38–40atrial tachycardia associated 66–7see also second degree heart block

atrioventricular nodal re-entry tachycardia(AVNRT) 81, 165

clinical scenario 183, 192, 192management 193see also junctional tachycardia

atrioventricular (AV) node 4, 58atrial fibrillation 76atrial tachycardia 66–7conduction problems 37–42nodal (junctional) escape 60, 61see also entries beginning junctional

axis see cardiac axis

B

Bazett’s formula 157bifascicular block 51, 52, 53, 161, 163, 176bifid P wave 86, 86, 111, 112, 112, 113

clinical scenario 183, 191, 192

sinus see sinus arrhythmiasupraventricular see supraventricular

rhythms ventricular see ventricular arrhythmia see also bradycardia; extrasystoles;

tachycardiaasymptomatic patient, ECG 105

atrial fibrillation 105, 106palpitations/syncope 151–63

normal ECGs 151–2patterns suggesting bradycardia 161patterns suggesting heart disease 152,

153patterns suggesting paroxysmal

tachycardia 152atheromatous plaque 129athlete(s)

ECG in 125, 126sinus bradycardia 107, 166

atrial contraction 56see also P wave

atrial escape 60, 61atrial escape beats 60atrial extrasystole 63, 65, 109, 112atrial fibrillation 76, 77, 78, 165

asymptomatic patient 105, 106carotid sinus pressure effect 82clinical scenario 182, 190–1management 191

atrial flutter 67, 68, 1652:1 block with 67, 68, 69carotid sinus pressure effect 72, 72, 82

atrial hypertrophy

Index

Note: Page numbers in bold refer to figures and tables.Abbreviations used in subentries: LBBB, left bundle branch block; RBBB, right bundle branch block.

Index

195

dizziness 164, 166bundle of His disease 180, 186–7

dual chamber pacing 169, 170

E

ECG12-lead 9–11normal see normal ECG role/aims 3

ECG recordercalibration see calibration electrical activity of leads 9leads see leads reports and interpretation 32–3times and speeds 6–8, 25, 27, 28–9, 30

see also paper speed ECG recordings 18, 19

abnormal, recognition features 83, 84analysis 56, 65, 82, 85, 103, 174, 175

order/method 65, 174basic principles 35‘clockwise rotation’ 19, 130, 137health screening use 105‘ideal’ 19, 20

see also normal ECG non-relaxed subject 27, 31normal see normal ECG paper, square size related to time 6, 7parts/components 4–5, 5, 7poor contact effect 23, 23–4practical points 19–32see also specific conditions

ectopic atrial rhythm 111, 111ectopic beats 63

see also extrasystolesejection systolic murmur 180, 186elderly

atrial fibrillation 191dizziness, heart rate 166

electrical interference 24, 24electrodes

number and positioning 9poor contact 23, 23–4reversal 19, 21

electrolyte abnormalitiesprolonged QT interval due to 157T wave abnormalities 101

enhanced automaticity 81escape rhythm/mechanism 60, 165, 177

atrial 60, 61complete heart block 41junctional 60, 61

carotid sinus pressure (CSP) 72, 72, 82, 193narrow complex tachycardia 164supraventricular tachycardia 72, 193

chest leads (V1–V6) see V1–V6 leadschest pain 128–44

cardiac ischaemia causing 130, 144causes 128, 128clinical scenario 179, 184, 185, 193constant, ECG features 128–42ECG features 128–46intermittent 144pulmonary embolism 148see also angina

chronic lung disease 19, 130, 137, 150,150

‘clockwise rotation’ 19, 130, 137coarctation of aorta 192‘compensatory’ pause, extrasystoles 65complete heart block see third degree

(complete) heart blockconducting bundle, accessory 79conduction problems 36–55, 176

AV node and His bundle 37–42clinical scenario 180, 186–7distal parts of left bundle branch 49–51in healthy people 112–15right/left bundle branches 43–8see also heart block

conduction system, of heart 4, 4, 36, 37constant chest pain 129–42coronary vasospasm 144

D

DC cardioversion 173, 193‘DDD’ pacing 169, 170defibrillation, cardiac arrest 173delta wave 79, 80depolarization and depolarizing wave 4,

13, 13, 36bundle branch block 43direction 4, 13, 43first degree heart block 37–8initiation, SA node 4, 56, 57, 60intrinsic frequency 59–60left bundle branch fascicles 49, 49pathways 49, 49supraventricular rhythms 58–9, 59upward/downward deflections 17, 35ventricular rhythms 59, 59

digoxin 101T wave inversion 101toxicity, management 191

block, heart see heart blockbradycardia 57, 59–60

intermittent 166, 168management 82–3pacing effect 82, 82sinus see sinus bradycardia syncope due to 161, 162, 163, 166

breathlessness 147–50causes 147, 147–50ECG features in 147–50heart disease causing 147lung disease causing 148

broad complex tachycardia see tachycardia,wide complex

Bruce protocol 144, 144bundle, accessory 79bundle branch block 43–8, 87

bilateral 43causes 117inverted T waves 45, 98, 98, 152mechanism 44supraventricular tachycardia with 75–6see also left bundle branch block (LBBB);

right bundle branch block (RBBB)bundle of His see His bundle

C

calcium, abnormal levels 101calibration, ECG recorder 8, 8, 24–5

over-calibration 24–5under-calibration 25, 26

cardiac arrest 172, 173causes 173nonshockable rhythms 173pulseless electrical activity (PEA) 173shockable rhythms 173

cardiac axis 14–16, 35deviation, causes 177left anterior fascicular block, effect 49, 50

with RBBB 51, 52, 54left axis deviation see left axis deviation measurement in degrees 16, 16normal 14, 16, 49, 50, 127right axis deviation see right axis

deviation right bundle branch block, effect 51, 52

with left anterior hemiblock 51, 52,54

significance 16cardiac ischaemia see ischaemia, cardiaccardiac rhythm see rhythm, cardiaccardiomyopathy, hypertrophic 152, 153

196

Index

slow/fast, causes 107heart sounds, second, widely split 180, 186high take-off ST segments 122, 122hemiblock

left anterior 49left posterior 51

His bundle 4, 79branches, anatomy 49, 49conduction problems 37–42disease, ECG 180, 186–7fibrosis 41

hyperkalaemia 101, 112, 125hypertrophic cardiomyopathy 152, 153hypertrophy, cardiac

ECG features 147see also left atrial hypertrophy; left

ventricular hypertrophy; rightatrial hypertrophy; rightventricular hypertrophy

hypokalaemia 101, 125, 190–1

I

idioventricular rhythm, accelerated 60, 63,164

infarction see myocardial infarctionintermittent bradycardia 166, 168intermittent chest pain see chest painintermittent tachycardia see paroxysmal

tachycardiainterventricular septum 17

depolarization from left to right 16, 35ischaemia, cardiac 144

acute chest pain 128, 130, 132, 144ECG role in diagnosis 128–9exercise-induced changes 97, 97lateral 91, 94normal ECG in 130ST segment depression 97, 130, 131see also angina; myocardial infarction

ischaemic pain 130see also chest pain

J

junctional escape 60, 61junctional extrasystole 63, 63, 64, 65junctional rhythm 58–9junctional tachycardia 70, 70, 71, 81

carotid sinus pressure effect 82see also atrioventricular nodal re-entry

tachycardia (AVNRT)

ventricular 60, 62exercise-induced ischaemic changes 97, 97exercise testing 144

abrasive pad use 23angina 144, 145, 146Bruce protocol 144, 144

extrasystoles 59, 63–6, 108–9, 178atrial 63, 63, 64, 65, 109, 112junctional 63, 63, 64, 65palpitations due to 159, 164, 165supraventricular 63, 64, 65, 65, 108, 165ventricular 64, 64, 108–9, 110, 164, 178

F

fibrillation 76–9see also atrial fibrillation; ventricular

fibrillationfirst degree heart block 37, 38, 54, 114,

162, 176causes 161in healthy people 112, 114treatment 54

flutter, atrial see atrial flutter

H

hair, poor electrode contact due to 23–4health screening, ECG usage 105healthy patients, ECG in 105–27

cardiac rhythm 105–11, 107conduction 112, 114QRS complex 116–21, 118, 119, 120,

121, 123, 124ST segment 122, 122, 123T wave 124, 124–5, 125see also normal ECG

heartconduction system 4, 4, 36, 37rhythm see rhythm, cardiac wiring diagram 4, 4, 37

heart block 37–42causes 161first degree see first degree heart block second degree see second degree heart

block third degree see third degree (complete)

heart block treatment 54

heart ratecalculation 6, 7normal 60paroxysmal tachycardia 164

L

leads 9, 10angles, and cardiac axis 16chest leads see V1–V6 leads limb leads see limb leads ‘standard’, ECG patterns 9–10, 10V leads see V1–V6 leadssee also cardiac axis; limb leads

left anterior hemiblock (left anteriorfascicular block) 49, 51, 93, 114,115, 176

effect on cardiac axis 49, 50RBBB with 51, 52, 54

treatment 54left atrial hypertrophy 86, 86, 147

clinical scenario 183, 191left axis deviation 15, 15, 16, 49, 50, 175,

187causes 177downward QRS complex and 114RBBB with 51, 52, 186, 187

treatment 54sinus rhythm with 51tachycardia with 76treatment 54ventricular tachycardia case 188, 188

left bundle branch 4anatomy 49, 49conduction problems in distal parts

49–51left bundle branch block (LBBB) 43, 45–6,

116, 176aortic stenosis and 190causes 117clinical scenario 182, 189first degree block and 162mechanism 44sinus rhythm with 48, 73, 75, 162stages 45, 45–6, 46treatment 54, 190

left posterior hemiblock 51left ventricle, influence on ECG pattern

16, 43left ventricular hypertrophy 118, 119, 147

clinical scenario 183, 191–2hypertrophic cardiomyopathy 153inverted T waves 90–1, 98management 192QRS complex 15, 90, 90–1, 118, 119summary of ECG features 147voltage criteria 90–1, 118, 191

left ventricular lead 17

Index

abnormal 85, 86, 175atrial escape 61atrial extrasystole 63, 63causes 102

absent 84atrial fibrillation 76, 77, 78junctional escape 61junctional extrasystole 63, 63–4junctional tachycardia 70, 70, 71ventricular tachycardia 74

arrhythmias with 83, 84in atrial extrasystoles 63, 63–4, 65, 112in atrial flutter with 2:1 block 67, 68, 69in atrial tachycardia 66bifid 112, 113, 183, 191, 192broad 86, 86, 175, 191

left atrial hypertrophy 86, 86, 191–2as distortion of T wave 38, 40ECG analysis questions 65faster ECG recorder speed effect 27healthy subjects 111inverted 111notched, broad 175peaked 86, 86, 88, 89, 102

pulmonary embolism 148, 149right atrial hypertrophy 86, 86

QRS ratio 177second degree block 186–7, 187tall 112in ventricular vs supraventricular

extrasystole 65–6pacemaker 169, 187

‘AAI’ 169atrial pacing 169, 171‘DDD’ 169, 170dual chamber pacing 169, 170functions/mechanisms 169operating mode (letters) 169ventricular pacing 169, 170‘VVI’ 169, 170

pain see chest painpalpitations 151, 159–73

ECG features 151–69normal ECGs 151–2with symptoms 164–6without symptoms 151–61

paper speed, ECG recorder 6, 24, 27, 28–912.5 mm/s (normal ECG) 3025 mm/s (normal ECG) 2050 mm/s (normal ECG) 24, 27, 28–9

Parkinson’s disease 27paroxysmal supraventricular tachycardia 164paroxysmal tachycardia 66, 152, 164–6

ECG patterns suggesting 152–60

limb leads 9, 10correct placement 19electrical activity 9, 19QRS complex 11, 13, 13reversed left/right leads 19, 21

limits of normal durations 127long QT interval 157, 157, 158

see also QT interval, prolongedLown–Ganong–Levine syndrome 152,

156, 156lung disease

breathlessness due to 148chronic 19, 130, 137, 150, 150pulmonary embolism 148, 148, 149

M

‘M’ pattern 190clinical scenario 182, 189–90, 190in LBBB 46, 48, 55, 156, 189–90

magnesium, abnormal levels 101midaxillary line 22, 22midclavicular line 22, 22mitral stenosis 112

bifid P wave 86, 86Mobitz type 1 (Wenckebach) block 38, 39,

39, 112, 140, 161Mobitz type 2 block 38, 39, 39, 161muscular activity, masking ECG 27, 31myocardial infarction 140, 141

accelerated idioventricular rhythm 60,63, 164

acute anterior 91, 92, 132, 133, 133, 134NSTEMI 100, 143

acute anterolateral 91, 93, 193, 193clinical scenario 184, 193left anterior hemiblock with 93

acute inferior 91, 94, 138development 98, 99

age of 92anterior NSTEMI 142–143broad complex tachycardia 75complete heart block 41development 98, 99diagnosis, criteria 129non-Q wave 98, 142

see also myocardial infarction, NSTEMI normal ECG initially 130, 142NSTEMI (subendocardial) 98, 100, 129,

142, 143old anterior 130, 135, 136old inferior 91, 92, 139

clinical scenario 181, 189

management 189old posterior 140, 141pain 128, 129, 130, 193posterior 91, 95, 140, 141Q wave see Q wave second degree heart block 140sequence of ECG changes 142, 193site of 142ST segment elevation see STEMI (ST

segment elevated myocardialinfarction)

STEMI see STEMI (ST segmentelevated myocardial infarction)

T wave inversion 98, 99, 100, 130ventricular tachycardia 75see also ischaemia, cardiac

myocardial ischaemia see ischaemia, cardiacmyocardial necrosis 129

N

narrow complex tachycardia 71, 82, 164nodal (junctional) escape 60, 61nodal (junctional) extrasystole 63, 63, 64, 65nodal (junctional) rhythm 58–9nodal (junctional) tachycardia 70, 70, 71, 81

carotid sinus pressure effect 82see also atrioventricular nodal re-entry

tachycardia (AVNRT)non-Q wave infarction 98, 142

see also myocardial infarction, NSTEMInon-ST segment elevation myocardial

infarction (NSTEMI) 98, 100, 129,142, 143

nonshockable rhythms, cardiac arrest 173,173

normal cardiac axis 14, 14, 16, 49, 50, 127normal ECG 5, 19, 20, 127, 151–2

clinical scenario 179, 185limits of normal durations 127paper speed variations 20, 25, 27,

28–9, 30at rest, in exercise testing 145variants 33, 33, 34, 35

NSTEMIs 98, 100, 129, 142, 143

O

over-calibration 25, 25

P

P wave 4, 5, 35, 56 197

198

Index

tachycardia, supraventricular/ventricular differentiation 75–6

ventricular rhythms 59ventricular tachycardia 73, 73, 181,

188, 188Wolff–Parkinson–White syndrome 79,

87, 156width abnormalities 87, 175

QT interval 7Bazett’s formula 157normal duration 127prolonged 8, 157, 157, 158

calcium abnormalities causing 101causes 157

QTc 157

R

R on T phenomenon 64, 64R wave 5, 5, 17, 87

acute anterolateral infarction 184, 193,193

dominant (V1) 118, 118in healthy people 118, 118–19left ventricular hypertrophy 119, 183,

192, 192old anterior infarction 130, 136old posterior infarction 140, 141pulmonary embolism and 148, 149secondary (R1) 44tall, in right ventricular hypertrophy 118transition point and 17, 19, 175

re-entry circuit 81, 81see also atrioventricular nodal re-entry

(AVNRE) tachycardiarecorder and recordings see ECG recorder;

ECG recordingsrepolarization 5

abnormal path 59, 98ventricular arrhythmias 59

reporting of ECG 32–3description sequence 32–3

reversal of electrodes 19, 21rhythm, cardiac 4, 56–84, 105–11

abnormal see arrhythmia analysis method 56, 65definition/use 4escape see escape rhythm/mechanism fast see tachycardia identification, lead used 11interpretation of ECG 36intrinsic 57junctional 58–9

‘torsade de pointes’ 157paroxysmal ventricular tachycardia 157, 164partial right bundle branch block 44, 116,

117percutaneous coronary intervention 129pericardial effusion 25pericarditis, elevated ST segment 96, 96–7posterior fascicle of left bundle branch 49,

49hemiblock 51

potassium, low/high levels 101, 125, 190–1PR interval 6, 7, 43

measurement 6normal 6–7, 7, 8, 37, 112, 127prolonged 37, 38, 112

see also heart block short 7, 152

Wolff–Parkinson–White syndrome 79,80

pre-excitation 79pre-excitation syndromes 152, 154premature contraction 63pulmonary embolism 89, 89–90, 148, 149,

175, 178summary of ECG changes 148

pulmonary hypertension 148, 152pulmonary oedema 188pulseless electrical activity (PEA) 173Purkinje fibres 4, 59

Q

Q wave 5, 5, 13, 87, 91–2, 178in healthy people 119–20, 120, 121infero-lateral, normal ECG with 120, 120in myocardial infarction 91, 119–20,

133, 134, 140, 142, 193acute anterolateral infarction 91, 184,

193, 193posterior infarction 140prevention 130, 142site, indication 178size 91, 102, 120, 178timing 98, 138see also STEMI (ST segment elevated

myocardial infarction) narrow 120normal 91, 178origin 91, 91–2in pulmonary embolism 90, 178‘septal’ 17, 17, 91, 126, 127, 178, 191–2STEMI, clinical scenario 181, 188–9,

189

summary of ECG patterns with 178width 91

QRS complex 5, 5, 35, 56, 175abnormal 85, 87–92, 175, 178

features and causes 83, 84, 102ventricular extrasystole 64, 64, 65

atrial fibrillation 76, 77, 78, 182, 190broadening see QRS complex,

wide/widening complete heart block 62concordance, in broad complex

tachycardia 188duration 7–8, 43, 87, 116, 127ECG analysis questions 65in healthy people 116–21, 118–24height 118, 175height increased 87–91, 101, 102, 119,

127, 175healthy subjects 118, 119, 119left ventricular hypertrophy 118, 119

in left ventricular hypertrophy 15, 90,90–1, 118, 119

limb leads 11, 13, 13narrow

atrial fibrillation, 182, 190supraventricular tachycardia 183,

192, 193normal 7, 7, 8, 127

characteristics 87duration 7–8, 43, 87, 116, 127supraventricular rhythms 59

P wave ratio 177paroxysmal tachycardia 164prolonged see QRS complex,

wide/widening in pulmonary embolism 89, 89–90in right ventricular hypertrophy 15, 87,

87–8, 88, 175shape 11–19, 13

factors influencing 16first, second and third stages 17, 17,

18in V leads 16–18, 17, 18

slurred upstroke,Wolff–Parkinson–Whitesyndrome 79, 80

transition point 17, 19, 175V leads 16–18, 17, 18ventricular escape rate 62wide/widening 8, 8, 59, 87, 116, 178

aortic stenosis and 182, 190bundle branch block 43, 87, 102causes 102, 178electrolyte abnormalities 101

Index

normal 56, 105–11, 127points/sites of initiation 58, 58sick sinus syndrome 160, 160, 161sinus see sinus rhythm slow see bradycardia supraventricular see supraventricular

rhythms ‘rhythm strip’ 11, 19, 20right atrial hypertrophy 86, 86, 88, 147, 149

tall P waves 112right axis deviation 15, 15, 16, 34, 51,

116, 175causes 177in healthy subjects 115in pulmonary embolism 148, 149in right ventricular hypertrophy 88

right bundle branch 4anatomy 49, 49

right bundle branch block (RBBB) 43, 44,46, 176

with both left bundle branches blockedsee third degree (complete) heartblock

cardiac axis, effect on 51, 52causes 117clinical scenario 180, 185–6in healthy people 116–18left anterior hemiblock with 51, 52

treatment 54management 54, 186partial 44, 116, 117pulmonary embolism and 148, 149QRS duration normal 43sinus rhythm with 47stages 44, 44, 45

right ventricular hypertrophy 118, 147,175, 178

inverted T waves 98, 152pulmonary embolism and 148QRS complex 15, 87, 87–8, 88QRS transition point 19summary of ECG features 147tall R wave 118

right ventricular lead 17R–R interval 6

chest pain scenario 179, 185heart rate association 7

RSR pattern 44, 46, 47, 55, 187clinical scenario 180, 186

S

S wave 5, 5, 45

in chronic lung disease 130, 137in right ventricular hypertrophy 87,

87–8, 88transition point and 17, 19wide, deep 44

‘S1Q3T3’ pattern 148second degree heart block 38–40, 39, 40,

54, 140, 1762:1 (‘two to one’) type 38, 39, 40, 161

atrial flutter with 67, 68, 693:1 (‘three to one’) type 38, 39, 1614:1 (‘four to one’) type 38, 39AV block with tachycardia vs 66–7causes 161clinical scenario 180, 186–7Mobitz type 1 phenomenon 38, 39, 39,

112, 140, 161Mobitz type 2 phenomenon 38, 39, 39,

161pacemaker for 187treatment 54, 187Wenckebach (Mobitz type 1)

phenomenon 38, 39, 39, 112,140, 161

second heart sound, widely split 180, 186‘septal’ Q wave 17, 17, 91, 126, 127, 178shivering, effect on ECG 27, 32shockable rhythms, cardiac arrest 173sick sinus syndrome 160, 160, 161, 166

ambulatory record 168sinoatrial disease 160, 160, 161sinoatrial (SA) node 4, 36, 56, 57

depolarization initiation 4, 56, 57, 60discharge rate 57, 60failure to depolarize 60

sinus arrhythmia 57, 57, 108clinical scenario 179, 185

sinus bradycardia 57, 58–9, 105athletes 107, 166causes 107

sinus rhythm 4, 56, 105with left axis deviation 51with left bundle branch block (LBBB)

48, 73, 75, 162with right bundle branch block (RBBB) 47

sinus tachycardia 57, 58–9, 105carotid sinus pressure in 82causes 107palpitations 152pulmonary embolism 148

skin cleansing, before ECG 23Sokolow–Lyon criteria 119speeds, ECG recorder 6–8, 24, 27, 28–9,

30

see also paper speed, ECG recorderST segment 5, 96, 141

abnormalities 96–7, 101, 175depressed 96, 97, 102, 178

angina 130, 144during exercise 97, 97in exercise testing 144horizontal, in ischaemia 122, 144ischaemia 97, 130, 131ischaemia, chest pain with 130, 144unstable angina 130, 131

downward-sloping 97, 101, 101clinical scenario 182, 190–1, 191nonspecific 122, 123

elevated 96, 96–7, 98, 102in healthy people 122, 122myocardial infarction see STEMI (ST

segment elevated myocardialinfarction)

evaluation 85in healthy people 122, 122, 123, 127high take-off 122, 122nonspecific changes 101, 122, 123normal 96, 96, 127

STEMI (ST segment elevated myocardialinfarction) 96–7, 98, 129, 130–40

acute anterior 132, 133, 133acute anterolateral 184, 193, 193acute inferior 138clinical scenario 184, 193complete heart block in 166diagnosis 130ECG details 130–40lateral infarction 142old anterior 130, 135, 136old inferior 139old posterior 141Q-wave infarctions 142sequence of ECG changes 142ST elevation, high take-off vs 122summary of changes 142

sternal angle 19Stokes–Adams attacks 187‘strain’ pattern 119subendocardial infarction 98

see also non-ST segment elevationmyocardial infarction (NSTEMI)

sudden death 129, 152, 157, 190supraventricular extrasystoles 64, 65, 65,

108, 165supraventricular rhythms 58, 58–9, 165

depolarization wave spread 59, 59types 165

supraventricular tachycardia 66–72, 192 199

200

Index

bundle branch block with 75–6carotid sinus pressure in 72, 72, 82clinical scenario 183, 192–3, 193management 193paroxysmal 164

symptomless patient see asymptomatic patientsyncope 151

due to bradycardia 161, 162, 163, 166due to tachycardia 164symptomless patient 151–63

T

T wave 5, 5abnormalities 59, 98–101, 175

causes 102electrolyte abnormalities causing 101

‘biphasic’ 98ECG analysis questions 65evaluation 85flattening 101, 102in healthy people 120, 121, 124, 124–5,

125, 127‘hyperacute’ changes 125inversion 98–101, 99, 100, 127, 178

causes 98, 102digoxin causing 101, 101ethnic factors affecting 124, 124, 127in healthy people 121, 121in left bundle branch block 45, 48,

98, 152in left ventricular hypertrophy 90–1,

98, 152, 191in myocardial infarction 98, 99, 100,

130in ‘old’ inferior infarction 181, 188–9,

189in pulmonary embolism 89, 89, 148,

149in STEMI 130in ventricular hypertrophy 88, 88, 90,

90–1, 98P wave as distortion 38, 40peaked 102, 175tall peaked 124–5, 125

tachycardia 57, 59, 66–76atrial see atrial tachycardia atrioventricular nodal re-entry see

atrioventricular nodal re-entrytachycardia (AVNRT)

broad complex see tachycardia, widecomplex

carotid sinus pressure in 72, 72, 82junctional (nodal) 70, 70, 71, 81, 82

see also atrioventricular nodal re-entrytachycardia (AVNRT)

left axis deviation with 76management 82–3narrow complex 71, 82, 164origin 81paroxysmal 66, 152, 164–6sinus see sinus tachycardia supraventricular see supraventricular

tachycardia syncope and 164ventricular see ventricular tachycardia wide complex 73, 73, 82, 152, 164, 166

clinical scenario 181, 188in Wolff–Parkinson–White syndrome 80,

81, 81third degree (complete) heart block 41, 42,

43, 62, 176bifascicular block with 51causes 161in STEMI 166treatment 54ventricular escape rhythm and 60, 62

thyrotoxicosis 191times and speeds, ECG recorder 6–8, 24,

27, 28–9, 30‘torsade de pointes’ 157, 159transition point. R and S waves equal 17, 19

shift, pulmonary embolism 89troponin 129, 129

U

U wave 5, 5, 101, 125, 176, 191hypokalaemia, atrial fibrillation 182, 190

under-calibration 25, 26unstable angina 129, 130

V

V1–V6 leads 10–11, 11, 12, 17, 35correct placement 19, 22, 22ECG patterns 10, 12, 18electrical activity 9, 9QRS complex 16–18, 17, 18relationship with heart 11transition point 19V1–V2 leads, right ventricle 11, 17V3–V4 leads, septum 11, 17V5–V6 leads, left ventricle 11, 17

Valsalva manoeuvre 193variants, of normal ECG 33, 33, 34, 35ventricular arrhythmia 58, 58, 59, 164

depolarization wave spread 59, 59ventricular contraction 57

see also QRS complexventricular escape 60, 62ventricular extrasystole 64, 64, 108–9,

110, 164, 178effects on following P wave 65, 66, 66summary of ECG features 164

ventricular fibrillation 79, 79, 159, 164induced by ventricular extrasystoles 64pulseless, shockable cardiac arrest 173

ventricular hypertrophy see left ventricularhypertrophy; right ventricularhypertrophy

ventricular pacing 170ventricular rhythms 164, 178

common 178ventricular tachycardia 73, 73, 74, 164, 167

carotid sinus pressure effect 83clinical scenario 181, 188heart rate for diagnosis 60myocardial infarction 75paroxysmal 164pulseless, shockable cardiac arrest 173supraventricular tachycardia with bundle

branch block vs 75–6‘torsade de pointes’ 157, 159

VF lead 9, 10VL lead 9, 10voltage changes, effect 90–1voltage criteria, left ventricular hypertrophy

90–1, 118, 191VR lead 9, 10, 14, 14‘VVI’ pacing 169, 170

W

‘W’ pattern 46, 48Wenckebach phenomenon 38, 39, 39, 112,

140, 161wiring diagram, of heart 4, 4, 37, 37Wolff–Parkinson–White (WPW) syndrome

75, 79–81, 80, 152sustained tachycardia 80, 81type A 154, 154, 156type B 154, 155, 156

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